Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

Effects of PAF and BN 52021 on cardiac function and regional blood flow in conscious rats

1989 ◽  
Vol 257 (1) ◽  
pp. H25-H32 ◽  
Author(s):  
A. L. Siren ◽  
G. Feuerstein
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Peripheral Resistance ◽  
Low Doses ◽  
Conscious Rats ◽  
High Doses

The effect of intravenous injections (0.1–3 nmol/kg) of platelet-activating factor (PAF) on blood pressure, heart rate, cardiac output, and blood flow (hindquarter, renal, mesenteric) were studied in conscious rats. PAF decreased blood pressure and total peripheral resistance (TPR) but increased heart rate; cardiac output was reduced by the highest dose. Low doses of PAF increased blood flow and decreased vascular resistance in all vascular beds, whereas high doses reduced mesenteric blood flow in part by increasing mesenteric vascular resistance. The hypotensive and cardiac effects of PAF were blocked by intravenous infusions of the selective PAF-receptor antagonists, 15 mg/kg BN 52021 and 1 mg/kg SDZ 63–441. BN 52021 also attenuated the hindquarter and renal responses to PAF, but the mesenteric responses remained relatively unchanged. The results indicate that PAF is a potent vasodilator of mesenteric greater than hindquarter = renal vessels at low doses and a cardiac depressant at high doses. A therapeutic role for the PAF antagonists BN 52021 and SDZ 63–441 is suggested in endotoxemia, anaphylaxis, and other disease states in which increased release of PAF contributes to key hemodynamic derangements.

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. H2511-H2517 ◽  
Author(s):  
Ming Yu ◽  
Venkat Gopalakrishnan ◽  
Thomas W. Wilson ◽  
J. Robert McNeill
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hemodynamic Responses ◽  
Hypertensive Group ◽  
Time Flow ◽  
Before And After ◽  
Vascular Responsiveness

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Regional distribution of blood flow during diving in the duck (Anas platyrhynchos)

1979 ◽  
Vol 57 (5) ◽  
pp. 995-1002 ◽  
Author(s):  
David R. Jones ◽  
Robert M. Bryan Jr. ◽  
Nigel H. West ◽  
Raymond H. Lord ◽  
Brenda Clark
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Regional Distribution ◽  
Peripheral Resistance ◽  
Tissue Blood Flow ◽  
Arterial Blood ◽  
The Brain

The regional distribution of blood flow, both before and during forced diving, was studied in the duck using radioactively labelled microspheres. Cardiac output fell from 227 ± 30 to 95 ± 16 mL kg−1 min−1 after 20–72 s of submergence and to 59 ± 18 mL kg−1 min−1 after 144–250 s of submergence. Mean arterial blood pressure did not change significantly as total peripheral resistance increased by four times during prolonged diving. Before diving the highest proportion of cardiac output went to the heart (2.6 ± 0.5%, n = 9) and kidneys (2.7 ± 0.5%, n = 9), with the brain receiving less than 1%. The share of cardiac output going to the brain and heart increased spectacularly during prolonged dives to 10.5 ± 3% (n = 5) and 15.9 ± 3.8% (n = 5), respectively, while that to the kidney fell to 0.4 ± 0.26% (n = 3). Since cardiac output declined during diving, tissue blood flow (millilitres per gram per minute) to the heart was unchanged although in the case of the brain it increased 2.35 times after 20–75 s of submergence and 8.5 times after 140–250 s of submergence. Spleen blood flow, the highest of any tissue predive (5.6 ± 1.3 mL g−1 min−1, n = 4), was insignificant during diving while adrenal flow increased markedly, in one animal reaching 7.09 mL g−1 min−1. The present results amplify general conclusions from previous research on regional distribution of blood flow in diving homeotherms, showing that, although both heart and brain receive a significant increase in the proportionate share of cardiac output during diving only the brain receives a significant increase in tissue blood flow, which increases as submergence is prolonged.

General and Regional Haemodynamic Effects of Intravenous Ergotamine in Man

1983 ◽  
Vol 65 (6) ◽  
pp. 599-604 ◽  
Author(s):  
P. Tfelt-Hansen ◽  
I.-L. Kanstrup ◽  
N. J. Christensen ◽  
K. Winkler
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Pressor Effect ◽  
Plasma Adrenaline ◽  
Vascular Beds

1. The effect of intravenous ergotamine on general (blood pressure and cardiac output) and regional (splanchnic, renal and muscular) haemodynamics was studied immediately and 3 h after administration in seven male volunteers. Also plasma catecholamines were determined. 2. An increase in blood pressure with a peak just after administration was observed. The cardiac output was unchanged and the pressor effect of ergotamine was due to an increase in total peripheral resistance. 3. Plasma noradrenaline decreased 65% at the peak of the pressor effect whereas plasma adrenaline was unchanged. 4. Hepatic blood flow decreased 34% just after ergotamine administration and was normal after 3 h. Renal blood flow decreased by 29 and 19%. Calf blood flow was unchanged. These results suggest that different vascular beds in man react differently to ergotamine.

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area

1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Lateral Hypothalamic Area ◽  
Hypothalamic Area ◽  
Pharmacological Blockade ◽  
Stimulation Of

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Atrial extract: hemodynamics in Wistar-Kyoto and spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. H265-H271 ◽  
Author(s):  
B. L. Pegram ◽  
M. B. Kardon ◽  
N. C. Trippodo ◽  
F. E. Cole ◽  
A. A. MacPhee
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Organ Blood Flow ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Atrial Natriuretic

Partially purified low (LMW) and high-(HMW) molecular-weight atrial natriuretic extracts were administered intravenously (540 micrograms protein/kg) to conscious Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Both LMW and HMW atrial natriuretic extracts produced an immediate decrease in mean arterial pressure that reached maximum within 5 min and returned to control levels within 30 min. In both strains, cardiac output decreased approximately 14% following administration of LMW. Total peripheral resistance increased only in SHR. Organ blood flow was significantly decreased to skin, brain, heart, kidneys, and splanchnic organs of WKY and to skin, muscle, heart, and splanchnic organs of SHR following administration of LMW. Corresponding increases in organ vascular resistance index were observed in brain, heart, and splanchnic organs of WKY and in skin, heart, and splanchnic organs of SHR. To some extent, the changes in organ blood flow may be a reflection of the decrease in cardiac output induced by LMW. After administration of HMW, no significant changes were observed in cardiac output or total peripheral resistance, although they tended to decrease. Organ vascular resistance was decreased to skin, muscle, brain, and splanchnic organs of SHR. Little difference was observed between WKY and SHR responses to atrial natriuretic extracts. These data indicate that atrial natriuretic extracts have an effect on systemic and regional hemodynamics in conscious rats that differs markedly from those of vasodilators such as nitroglycerin or hydralazine.

The Effect of Dietary Sodium Intake on the Blood Pressure and Cardiac Output Responses to Angiotensin II in Unanaesthetized Rats

1977 ◽  
Vol 52 (6) ◽  
pp. 571-576
Author(s):  
Barbara L. Slack ◽  
J. M. Ledingham
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Dose Response ◽  
Sodium Intake ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Response Curves ◽  
Low Sodium ◽  
Dose Response Curves

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium and administered in various sequences. 2. Dose—response curves were shifted to the left in rats on a high-, compared with a low-, sodium intake. This response was maintained for 7 days on changing from high to low sodium. 3. There was no difference in the relation between the fall of cardiac output and the rise of blood pressure in any of the experimental groups. 4. Dose—response curves for peripheral resistance showed the same directional change as seen for the pressor response in rats on high- and low-sodium diets. Since depression of cardiac output was proportional to the pressure rise, the absolute change in peripheral resistance was greater than the blood pressure response. The proportional changes were similar. 5. It is concluded that alterations in the pressor response to angiotensin caused by changes in sodium loading are attributable to changes in peripheral resistance and not to changes in the cardiac output response to the acute rise in blood pressure.

Cardiovascular response to acute hypocapnia due to overbreathing

1964 ◽  
Vol 206 (5) ◽  
pp. 1025-1030 ◽  
Author(s):  
Robert C. Little ◽  
Charles W. Smith
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Artificial Respiration ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Fixed Rate ◽  
Essential Change

Anesthetized dogs were maintained by artificial respiration at a fixed rate and depth. The composition of inspired CO2 was varied while O2 content was maintained at control levels. Cardiac output was measured by the indicator-dilution technique. Acute reduction of end-expiratory CO2 levels below the normal value caused a decrease in blood pressure, pulse pressure, stroke volume, and cardiac output, no essential change in heart rate and an increase in total peripheral resistance. Mean systemic blood pressure and net vascular resistance were less with hypocapnia than they were at the same cardiac output at normal CO2 levels. However, the over-all vascular resistance was greater with hypocapnia than it was in the same animal at normal CO2 levels and control output values. Analysis of these data leads to the conclusion that the hypocapnia produced by overbreathing causes some degree of net vasodilation. The hypotension associated with hyperventilation appears to result in these experiments from the drop in cardiac output and to a lesser degree the relatively less than normal compensatory increase in total peripheral resistance.

Time-Course of Vascular Resistance Changes in Mineralocorticoid Hypertension of Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 97s-100s ◽  
Author(s):  
G. J. Wenting ◽  
A. J. Man in 'T Veld ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Plasma Volume ◽  
High Resistance ◽  
Total Peripheral Resistance ◽  
Extracellular Volume ◽  
Peripheral Resistance ◽  
High Flow ◽  
Mean Blood Pressure

1. Repeated measurements of blood pressure, cardiac output (99mTc-labelled albumin dilution with single-probe precordial counting of radioactivity), plasma volume and extracellular volume were made in 20 subjects exposed to mineralocorticoid excess. Patients with aldosterone-producing adenoma (n = 14) were followed for 6 weeks during the recurrence of hypertension after spironolactone treatment had been stopped. Patients with adrenal insufficiency (n = 4) were followed for 6–9 weeks after treatment with dexamethasone (1 mg daily) and fludrocortisone (0.5 mg daily) was begun. Patients with severe orthostatic hypotension due to autonomic insufficiency (n = 2) were followed for 21 and 120 weeks while treated with fludrocortisone (0.25 mg daily). Measurements were made weekly during the first 6 weeks and with longer intervals thereafter. 2. All subjects showed increments of cardiac output, stroke volume, plasma volume and extracellular volume during the first 2 weeks with little or no increase in total peripheral resistance. Mean blood pressure rose from 104 ± 3 to 126 ± 5 mmHg (mean ± sem) (P < 0.001, n = 14) in that period in primary aldosteronism and from 85 ± 4 to 94 ± 6 mmHg (P > 0.05, n = 6) with fludrocortisone. 3. After 6 weeks hypertension was maintained by increased resistance in nine subjects, whereas cardiac output and plasma volume had returned towards normal (mean blood pressure at the end of the study 127 ± 4 mmHg). In the remainder hypertension was maintained by increased cardiac output and expanded plasma Volume for at least 6 weeks (mean blood pressure at the end of the study 131 ± 8 mmHg). The patients with the high-resistance pattern were older (56 ± 2 years) than the patients with the high-flow pattern (34 ± 2 years) (P < 0.01). 4. Mean blood pressure and extracellular fluid volume were positively correlated (r = 0.63, P < 0.001, n = 161). Cardiac output was positively correlated with plasma volume (r = 0.51, P < 0.001, n = 161), and total peripheral resistance was inversely correlated with the plasma volume/interstitial fluid volume ratio (r = 0.47, P < 0.001, n = 161). 5. The long duration of a high-flow state and the interindividual differences in progression of high-resistance hypertension argue against a cause-and-effect relation between flow and resistance through local metabolic factors (auto-regulation) as a hypertensive mechanism in sodium loading. The results are compatible with the view that fluid-shifts between the intravascular and extravascular compartments can influence the changes in cardiac output and resistance in early and sustained hypertension due to sodium overload. Cardiac output is increased when the proportion of fluid that is retained in the intravascular compartment is relatively high, and vascular resistance is increased when that proportion is relatively low.

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