Abstract P222: Venous Dilation Contributes to 5-HT-induced Hypotension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Imaging System ◽  
Isometric Force ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Mesenteric Arteries ◽  
Conscious Rat ◽  
Cross Sectional ◽  
Induced Hypotension ◽  
Vascular Bed

Serotonin (5-hydroxytryptamine, 5-HT) infusion in a normal conscious rat decreases mean arterial pressure (MAP), in part by reduction in total peripheral resistance. Microsphere experiments have shown 5-HT increases blood flow within the splanchnic vascular bed, with the greatest being in the intestine and spleen. Interestingly, 5-HT does not cause a direct relaxation of resistant (small or large) mesenteric arteries. The present study addresses the possibility of the venous circulation contributing to the 5-HT induced fall in blood pressure. Our working hypothesis is venous dilation, specifically dilation of veins measurable within the splanchnic vascular bed, contributes to 5-HT-induced hypotension. Using an ultrasound imaging system (Vevo 2100 imaging system; 21 MHz probe,Visual Sonics Inc.), telemetry-implanted, anesthetized male Sprague Dawley rats underwent cross-sectional imaging which was controlled for respiration and cardiac cycles. The following vessels were imaged: abdominal aorta (AA); portal vein (PV); abdominal inferior vena cava (IVC); and superior mesenteric vein (SMV). Following the collection of baseline MAP and vessel diameter measurements, Alzet osmotic mini-pumps containing vehicle (saline; n=9) or 5-HT (25 ug/kg/min; n=9) were implanted for 1 week. After, 24 hours of infusion, 5-HT increased the vein diameter (SMV 17.48±2%; PV 17.67±2%; IVC 46.87±8%) and maintained the AA diameter ( AA 0.93±1%) from baseline while reducing MAP (vehicle 101.93±3; 5-HT 84.68±2 mm Hg; p<0.05).One-week post removal of all osmotic mini-pumps, there was no difference in the MAP or diameter of all noted vessels between the two treatment groups. To correlate with in vivo findings, the PV and IVC, when isolated in a tissue bath for measurement of isometric force and contracted with endothelin 1, relaxed in a concentration dependent fashion to 5-HT and 5-carboxamidotryptamine (5-HT 1/7 receptor agonist;1 nM-10 uM). Collectively, these findings highlight the contribution of splanchnic venous dilation in 5-HT-induced hypotension and propose a possible mechanism for 5-HT reduction in blood pressure.

Cardiovascular reflexes during abdominal ischemia in cats

1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Vena Cava ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Cardiovascular Reflexes ◽  
Group 3

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.

Role of vasopressin in acutely altered baroreflex sensitivity during hemorrhage in rats

1991 ◽  
Vol 261 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
B. L. Brizzee ◽  
R. D. Russ ◽  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Blood Loss ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Arterial Hemorrhage ◽  
Moderate Elevation

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.

scholarly journals Ethnicity-Specific Changes in Cardiac Troponin T in Response to Acute Mental Stress and Ethnicity-Specific Cutpoints for the R Wave of the aVL Lead

2019 ◽  
Vol 188 (8) ◽  
pp. 1444-1455 ◽  
Author(s):  
Annemarie Wentzel ◽  
Leoné Malan ◽  
Roland von Känel ◽  
Nicolaas T Malan
Keyword(s):  
Blood Pressure ◽  
Stress Responses ◽  
Cardiac Troponin ◽  
Mental Stress ◽  
Troponin T ◽  
Myocardial Strain ◽  
Peripheral Resistance ◽  
Cardiac Troponin T ◽  
Cross Sectional ◽  
Cardiac Stress

Abstract Acute mental stressor–induced cardiac stress responses might contribute to excessive myocardial strain and resultant cardiovascular episode risk. We assessed ethnicity-specific acute cardiac stress (by measuring cardiac troponin T (cTnT) and N-terminal prohormone of brain natriuretic peptide) related to hemodynamic activity. The prospective Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study was conducted during 2007–2008 in South Africa. In the cross-sectional phase of the SABPA study, 388 black and white participants underwent a 1-minute acute mental stressor, during which blood pressure was continuously measured. Fasting blood samples for cardiac stress markers were obtained before and 10 minutes after stress (% change). Resting 10-lead electrocardiogram measured the R wave of the aVL lead (RaVL). Black participants exhibited greater cardiac stress responses (P &lt; 0.001), diastolic blood pressure, total peripheral resistance, and stroke volume compared with white participants, who displayed decreases in cardiac stress and increases in cardiac output. Prestress and stressor cTnT cutpoints of 4.2 pg/mL predicted 24-hour, daytime, and nighttime diastolic hypertension in black participants (P &lt; 0.001). These cTnT cutpoints were associated with an ethnicity-specific RaVL cutpoint of 0.28 mV (odds ratio = 3.49, 95% confidence interval: 2.18, 5.83; P = 0.021). Acute mental stress elicited an α-adrenergic activation pattern and cardiac stress hyperreactivity only in black participants. Mental stress might increase the black population’s risk for ischemic episodes and heart disease.

Abstract 352: Evaluation of Structural, Mechanical and Functional Properties in Small Arteries of Spontaneously Hypertensive Rats Before and After the Development of High Blood Pressure.

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Rafael M Jeuken ◽  
Luciana V Rossoni
Keyword(s):  
Blood Pressure ◽  
Mesenteric Arteries ◽  
Intraluminal Pressure ◽  
Cross Sectional ◽  
Spontaneously Hypertensive ◽  
Wall Stiffness ◽  
Before And After ◽  
Wistar Kyoto ◽  
Picrosirius Red

Structural, mechanical and functional adjustments occur in small mesenteric arteries (SMA) of hypertensive models. However, the role of these properties to trigger hypertension is unknown. As expected, the systolic blood pressure was higher in adult (A, 6-month old) male SHR as compared to Wistar-Kyoto rats (WKY) (WKYA: 125±1.1 vs SHRA: 187±3.3 mmHg*); however, it was similar in young (Y, 6-week old) SHR as compared to age-matched WKY (WKYY: 117±1.8 vs SHRY: 120±2.1 mmHg). The 3rd order mesenteric arteries were mounted in a pressure myograph to analyze the structural [lumen diameter (L), cross sectional area (CSA), wall/lumen ratio (W/L)] and mechanical properties [β, representing wall stiffness]. Endothelium-dependent relaxation to acetylcholine (ACh, 10-10-10-5 M) or -independent relaxation to sodium nitroprusside (SNP, 10-9-10-4 M) were evaluated in SMA using wire myography. At the passive condition (Ca2+-free solution) and intraluminal pressure of 160 mmHg, the L was lower in SMA of both SHR (WKYY: 294±12.0 vs SHRY: 241±4.3*; WKYA: 353±4.7 vs SHRA: 283±6.2 μm*); while the W/L ratio was higher in SHR as compared to age-matched WKY. CSA was similar between age-matched groups. β value was higher in SHR independently of age (WKYY: 5.8±0.4 vs. SHRY: 7.8±0.4*; WKYA: 4.7±0.1 vs SHRA: 6.7±0.4*). The collagen area evaluated by picrosirius red staining was higher in SMA of SHRA as compared to WKYA (WKYA: 15±2.4 vs SHRA: 26±1.8%*), but it did not change in young rats. ACh-induced maximal relaxation was similar in SMA from young groups (WKYY: 93±3.8 vs SHRY: 92±3.1%); however, in SHRA ACh elicited a biphasic curve inducing contraction at concentrations higher than 10-7M, which was not observed in WKYA. Relaxation to SNP did not change among groups. Reactive oxygen species analyzed by dihydroethidium was higher in SMA of SHRA as compared to WKYA (WKYA: 100±3.7 vs SHRA: 126±10.3% of integrated density*), but did not change in young SMA. Although SMA of SHRY present eutrophic inward remodeling and wall stiffening, it does not present collagen deposition, oxidative stress or endothelial dysfunction as observed in SHRA; suggesting that vascular remodeling and wall stiffness of SMA are not sufficient to trigger hypertension, at least when endothelial function is preserved.

Abstract 202: Activation of Cyp4a12-20-HETE Synthase Increases Blood Pressure and Promotes Vascular Hypertrophy and Cardiac Dysfunction

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Gregory Joseph ◽  
Yan Ding ◽  
Victor Garcia ◽  
Elisabeth Steadman ◽  
Jorge Capdevila ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Dysfunction ◽  
Peripheral Resistance ◽  
Sectional Area ◽  
Cross Sectional ◽  
Microvascular Remodeling ◽  
Lv Volume ◽  
Smooth Muscle Contractions

20-Hydroxyeicosatetraenoic acid (20-HETE) is a microcirculatory cytochrome P450-derived eicosanoid shown to increase smooth muscle contractions and proliferation, stimulate endothelial dysfunction and activation, and promotes hypertension. We developed a mouse model (Cyp4a12tg) in which the expression of Cyp4a12, the sole 20-HETE synthase in mouse, is under the control of the doxycycline (DOX) promoter. Administration of DOX to Cyp4a12tg mice increased blood pressure (131±3 vs 100±2 mmHg, p<0.05), which was prevented by co-treatment with the 20-HETE antagonist, 20-HEDGE (96±3 mmHg, p<0.05). Media-to-lumen ratio and medial cross sectional area of renal microvessels from DOX-treated Cyp4a12tg mice significantly increased compared to untreated (M/L, 0.15±0.01 vs 0.07±0.01; mCSAx103 10.8±0.92 vs. 6.4±0.48 mm2); these increases were abolished by co-treatment with 20-HEDGE. Cardiac output and heart rate were unchanged, whereas %EF and %FS were reduced and LV volume and diameter at systole increased in DOX-treated Cyp4a12tg. Total peripheral resistance (TPR) was significantly increased in DOX-treated Cyp4a12tg mice (8.00±0.39 vs 6.77±0.36 mmHg/ml/min, p<0.05); co-treatment with 20-HEDGE decreased (p<0.0%) DOX-induced TPR in Cyp4a12tg mice (7.45±0.22 mmHg/ml/min). These results indicate that activation of Cyp4a12-20-HETE synthase causes hypertension, microvascular remodeling, and cardiac dysfunction. The results also suggest that 20-HETE promotes hypertension by increasing TPR. However, the mechanisms underlying Cyp4a12-20-HETE-driven microvascular remodeling and cardiac dysfunction are yet to be explored.

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

1995 ◽  
Vol 269 (1) ◽  
pp. G153-G159 ◽  
Author(s):  
L. V. Kuznetsova ◽  
D. Zhao ◽  
A. M. Wheatley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
Suture Technique ◽  
Arterial Blood Flow ◽  
Conscious Rat ◽  
Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to hypoxia and hypercapnia in barodenervated rats

1990 ◽  
Vol 68 (2) ◽  
pp. 678-686 ◽  
Author(s):  
B. R. Walker ◽  
B. L. Brizzee
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Conscious Rat ◽  
Hypercapnic Hypoxia ◽  
Intact Rats

Experiments were performed to examine the role of the arterial baroreceptors in the cardiovascular responses to acute hypoxia and hypercapnia in conscious rats chronically instrumented to monitor systemic hemodynamics. One group of rats remained intact, whereas a second group was barodenervated. Both groups of rats retained arterial chemoreceptive function as demonstrated by augmented ventilation in response to hypoxia. The cardiovascular effects to varying inspired levels of O2 and CO2 were examined and compared between intact and barodenervated rats. No differences between groups were noted in response to mild hypercapnia (5% CO2); however, the bradycardia and reduction in cardiac output observed in intact rats breathing 10% CO2 were eliminated by barodenervation. In addition, hypocapnic hypoxia caused a marked fall in blood pressure and total peripheral resistance (TPR) in barodenervated rats compared with controls. Similar differences in TPR were observed between the groups in response to isocapnic and hypercapnic hypoxia as well. It is concluded that the arterial baroreflex is an important component of the overall cardiovascular responses to both hypercapnic and hypoxic stimuli in the conscious rat.

Abstract P617: Actions on the Splanchnic Venous System Contribute to 5-HT-induced Hypotension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Hannah Garver ◽  
Gregory D Fink ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Portal Vein ◽  
Receptor Antagonist ◽  
Portal Pressure ◽  
Vena Cava ◽  
Systemic Blood Pressure ◽  
Venous System ◽  
Systemic Blood ◽  
Induced Hypotension ◽  
Arterial Blood

Infusion of serotonin (5-hydroxytryptamine, 5-HT) into conscious normotensive and hypertensive rats causes a sustained reduction in systemic blood pressure. Imaging studies reveal that the blood pressure fall is closely associated with dilation of the large splanchnic veins (mesenteric, portal and abdominal vena cava), suggesting that active venodilation contributes to the fall in blood pressure. In fact, isolated splanchnic veins dilate directly to 5-HT via activation of the 5-HT 7 receptor, and a 5-HT 7 receptor antagonist prevents the 5-HT induced fall in blood pressure. To determine if the splanchnic venodilation caused by 5-HT is active or passive, anesthetized male Sprague Dawley rats were instrumented with arterial and venous lines for pressure measurements and 5-HT administration, respectively, while splanchnic veins were imaged using the Vevo® 2100 Ultrasound system. Measures were made relative to baselines measures. Within 5 minutes of infusion, 5-HT (25 ug/kg/min) caused an initial fall in portal vein pressure (~8-10% reduction) accompanied by dilation of the portal vein (~40% increase). No changes were seen in the dimensions or pressure of the abdominal vena cava at this time. Mean arterial blood pressure was reduced (>40% reduction). All of these changes were prevented by pretreatment with the 5-HT 7 receptor antagonist SB269970. SB269970 during 5-HT infusion also caused an immediate reversal of changes in blood pressure and venous dimensions. Thus, active dilation of the pre-hepatic splanchnic venous system may be an early cause of 5-HT-induced hypotension. A more chronic experiment was performed in rats that were instrumented with a new dual channel radiotelemeter for concomitant measure of systemic and portal pressure in the conscious state. Within one hour after initiation of 5-HT infusion, portal venous pressure was elevated 38±0.2% above baseline (n=3) versus vehicle infused animals (4±0.3% above baseline; n=3), suggesting an action of 5-HT on intrahepatic venous resistance. Within 24 hours, portal pressure elevation resolved but blood pressure remained reduced. Collectively these data highlight the portal venous circulation as an important site of action for 5-HT in causing acute and chronic falls in systemic blood pressure.

Estrogen replacement attenuates resistance artery adrenergic sensitivity via endothelial vasodilators

1997 ◽  
Vol 272 (5) ◽  
pp. H2264-H2270 ◽  
Author(s):  
M. C. Meyer ◽  
K. Cummings ◽  
G. Osol
Keyword(s):  
Blood Pressure ◽  
Peripheral Resistance ◽  
Mesenteric Arteries ◽  
Muscarinic Agonist ◽  
Estrogen Replacement ◽  
Resistance Artery ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Adrenergic Stimulation

The objective of this study was to determine whether chronic estrogen replacement alters adrenergic constriction and endothelium-dependent dilation in resistance arteries from the rat. Resistance-sized (< 200 microns) mesenteric arteries from castrated female Sprague-Dawley rats with (E2; 21 day, 0.5-mg pellet) and without (OvX) estrogen replacement were removed for in vitro study on a pressurized arteriograph system. Sensitivity to alpha-adrenergic constriction and the role of the endothelium in its modulation and of agonist-provoked endothelium-dependent relaxation were determined. Estrogen-treated rats had decreased heart rate as well as systolic and diastolic blood pressure. Arteries from estrogen-replaced rats were fivefold less sensitive to alpha 1-adrenergic stimulation with phenylephrine (50% effective concentration: E2, 3.2 +/- 1.1 microM; OvX, 0.6 +/- 0.2 microM; P < 0.05). This difference was abolished by endothelial denudation, blockade of cyclooxygenase (1 microM ibuprofen), or nitric oxide synthase blockade (0.24 mM N omega-nitro-L-arginine). There was no difference in muscarinic agonist-provoked relaxation or vascular smooth muscle sensitivity to prostacyclin or sodium nitroprusside. These results indicate that estrogen replacement decreases resistance artery adrenergic sensitivity by increasing the basal release of relaxing factors from the endothelium. This effect on small artery function may produce dual cardioprotective effects by decreasing peripheral resistance, blood pressure, and the likelihood of thrombosis.

Effects of converting-enzyme inhibitor on hemodynamic actions of ANP in renal hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. R365-R369
Author(s):  
M. G. Salom ◽  
F. J. Fenoy ◽  
A. C. Ingles ◽  
L. Martinez ◽  
T. Quesada
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Hemodynamic Effects ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Induced Hypotension ◽  
Renal Hypertensive Rats

In the present study, we have evaluated whether the hemodynamic effects of atrial natriuretic peptide (ANP) infusion in two-kidney, one-clip (2K, 1C) hypertensive rats are mediated by inhibition of the renin-angiotensin system (RAS). Hemodynamic determinations were performed by thermodilution in conscious, chronically instrumented animals. ANP (1.5 micrograms.kg-1.min-1) and converting-enzyme (CE) inhibitor captopril (1 mg/kg plus 1 mg.kg-1.h-1), produced a similar fall of blood pressure through different hemodynamic mechanisms. ANP induced hypotension by decreasing cardiac index (CI; from 337.3 +/- 24.9 to 255.1 +/- 21.3 ml.min-1.kg-1, P less than 0.001), whereas a fall in total peripheral resistance (TPR) was observed during CE inhibition (from 0.568 +/- 0.02 to 0.488 +/- 0.02 mmHg.min.ml-1.kg, P less than 0.05). In addition, the ANP-induced decrease in CI was not significantly modified by previous CE inhibition. Furthermore, the decrease in TPR induced by CE inhibition did not change when CE inhibitor was administered during ANP treatment. The results of the present study indicate that the acute hemodynamic responses to ANP in 2K, 1C hypertensive rats are not mediated through antagonism of the vasoconstrictor actions of the RAS.

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