AT1 receptor block does not affect arterial baroreflex during pregnancy in rabbits

2001 ◽  
Vol 280 (5) ◽  
pp. H1996-H2005 ◽  
Author(s):  
Kathleen P. O'Hagan ◽  
Kara A. Skogg ◽  
Jennifer B. Stevenson
Keyword(s):  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Sympathetic Response ◽  
Reflex Gain ◽  
Receptor Block ◽  
Renal Sympathetic

The role of ANG II in the arterial baroreflex control of renal sympathetic nerve activity (RSNA) in eight term-pregnant (P) and eight nonpregnant (NP) conscious rabbits was assessed using sequential intracerebroventricular and intravenous infusions of losartan, an AT1 receptor antagonist. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Pregnant rabbits exhibited a lower maximal RSNA reflex gain (−44%) that was primarily due to a reduction in the maximal sympathetic response to hypotension (P, 248 ± 20% vs. NP, 357 ± 41% of rest RSNA, P < 0.05). Intracerebroventricular losartan decreased resting BP in P (by 9 ± 3 mmHg, P < 0.05) but not NP rabbits, and had no effect on the RSNA baroreflex in either group. Subsequent intravenous losartan decreased resting BP in NP and further decreased BP in P rabbits, but had no significant effect on the maximal RSNA reflex gain. ANG II may have an enhanced role in the tonic support of BP in pregnancy, but does not mediate the gestational depression in the arterial baroreflex control of RSNA in rabbits.

Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity

2002 ◽  
Vol 282 (5) ◽  
pp. H1592-H1602 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Short-term intravenous infusion of angiotensin II (ANG II) into conscious rabbits reduces the range of renal sympathetic nerve activity (RSNA) by attenuating reflex disinhibition of RSNA. This action of ANG II to attenuate the arterial baroreflex range is exaggerated when ANG II is directed into the vertebral circulation, which suggests a mechanism involving the central nervous system. Because an intact area postrema (AP) is required for ANG II to attenuate arterial baroreflex-mediated bradycardia and is also required for maintenance of ANG II-dependent hypertension, we hypothesized that attenuation of maximum RSNA during infusion of ANG II involves the AP. In conscious AP-lesioned (APX) and AP-intact rabbits, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between mean arterial blood pressure (MAP) and RSNA. Intravenous infusion of ANG II into AP-intact rabbits resulted in a dose-related attenuation of maximum RSNA observed at low MAP. In contrast, ANG II had no effect on maximum RSNA in APX rabbits. To further localize the central site of ANG II action, its effect on the arterial baroreflex was assessed after a midcollicular decerebration. Decerebration did not alter arterial baroreflex control of RSNA compared with the control state, but as in APX, ANG II did not attenuate the maximum RSNA observed at low MAP. The results of this study indicate that central actions of peripheral ANG II to attenuate reflex disinhibition of RSNA not only involve the AP, but may also involve a neural interaction rostral to the level of decerebration.

Increase in sympathetic activity with age. I. Role of impairment of arterial baroreflexes

1991 ◽  
Vol 260 (4) ◽  
pp. H1113-H1120 ◽  
Author(s):  
G. Hajduczok ◽  
M. W. Chapleau ◽  
S. L. Johnson ◽  
F. M. Abboud
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Conscious State ◽  
Bolus Administration ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

The purpose of this study was to evaluate changes in arterial baroreflex function with aging. Mean arterial pressure (MAP) obtained in the awake state was 110 +/- 7 mmHg in the young animals (1 yr; n = 5) and 128 +/- 6 mmHg in the old beagles (11 yr; n = 11) (P less than 0.05). In response to bolus administration of varying doses of phenylephrine and nitroglycerin in the conscious state, the slope relating heart rate (HR) to MAP was attenuated significantly in the old animals compared with the young (-0.87 +/- 0.30 vs. -2.35 +/- 0.44 beats.min-1.mmHg-1; P less than 0.05). After atropine, the baroreflex control of HR was abolished in both groups. After anesthesia and sectioning of the aortic depressor nerves, and with isolated carotid sinus pressures (CSP) held at 50 mmHg, absolute renal sympathetic nerve activity (RSNA) was significantly greater in the old (368 +/- 40 Hz) vs. the young animals (41 +/- 9 Hz). In the old, the gains of baroreflex inhibition of MAP (0.78 +/- 0.09) and normalized RSNA (0.38 +/- 0.14%/mmHg) during increases in CSP were decreased significantly compared with the young (MAP, 1.16 +/- 0.17 mmHg, and RSNA, 0.72 +/- 0.06%/mmHg). In a subgroup of old normotensive animals (n = 5), the baroreflex gain of RSNA was still attenuated (0.43 +/- 0.11%/mmHg) compared with the young. The reflex reduction in absolute RSNA as a function of baseline RSNA was also impaired in old vs. young beagles.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial baroreflex during pregnancy and renal sympathetic nerve activity during parturition in rabbits

1998 ◽  
Vol 274 (5) ◽  
pp. H1635-H1642 ◽  
Author(s):  
Kathleen P. O’Hagan ◽  
Susan M. Casey
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Reflex Gain ◽  
Maximal Gain ◽  
Renal Sympathetic

The arterial baroreflex control of renal sympathetic nerve activity (RSNA) was evaluated in nine term pregnant (P) and 12 nonpregnant (NP) conscious New Zealand White rabbits. In an additional four P rabbits, the RSNA response to spontaneous parturition was measured. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Rest BP (P: 61 ± 2 vs. NP: 73 ± 2 mmHg) and the centering point of the baroreflex (P: 57 ± 2 vs. NP: 70 ± 2 mmHg) were lower ( P < 0.05) in term pregnancy. Baroreflex range (P: 246 ± 14% vs. NP 263 ± 24% of rest RSNA) was not affected by pregnancy. However, maximal reflex gain was moderately depressed (−44%) in P rabbits (P: −15 ± 1 vs. NP: −27 ± 4% of rest RSNA/mmHg; P < 0.05) due to a significant reduction in the slope coefficient. Delivery of a fetus was associated with strong renal sympathoexcitation. Peak RSNA averaged 80 ± 37% of smoke-elicited RSNA or 1,221 ± 288% of rest RSNA (mean ± SD). These results suggest that, in contrast to rat pregnancy, depressed arterial baroreflex control of RSNA in rabbit pregnancy is due primarily to a reduction in maximal gain rather than a reduction in the maximal sympathetic response to hypotension.

Effects of pregnancy and progesterone metabolites on arterial baroreflex in conscious rats

1997 ◽  
Vol 272 (3) ◽  
pp. R924-R934 ◽  
Author(s):  
S. Masilamani ◽  
C. M. Heesch
Keyword(s):  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Progesterone Metabolites ◽  
Progesterone Metabolite ◽  
In Pregnancy ◽  
Renal Sympathetic

Previous experiments in anesthetized rats suggested that sympathoexcitatory responses were attenuated in pregnant (P) rats. The major progesterone metabolite, 3alpha-hydroxy-dihydroprogesterone (3alpha-OH-DHP), is elevated in pregnancy and reportedly potentiates central gamma-aminobutyric acidergic mechanisms, whereas the 3beta-isomer (3beta-OH-DHP) is inactive. This study obtained baroreflex curves in conscious rats by recording reflex changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) due to perturbations in mean arterial pressure (MAP) [i.v. phenylephrine (PE) and nitroprusside (NTP)] in P rats and in virgin (V) rats before (control) and 15 min after infusion (i.v.) of 3alpha-OH-DHP or 3beta-OH-DHP. Baseline MAP was lower in P rats (P = 102 +/- 2 vs. V = 124 +/- 3 mmHg). Compared with V rats, P rats exhibited less "sympathetic reserve" to respond to a hypotensive challenge, as evidenced by decreased maximum NA and decreased slope of RSNA baroreflex responses to NTP. However, HR baroreflex curves were similar in P and V rats. Acute intravenous administration of 3alpha-OH-DHP to conscious V rats mimicked the effects of pregnancy. Baroreflex sympathoexcitatory responses were decreased, whereas baroreflex control of HR was unaffected. The 3beta-isomer of DHP had no effect on NA or HR baroreflex responses. These results suggest that pregnancy may have differential effects on baroreflex control of sympathetic outflow and HR, and the major metabolite of progesterone, 3alpha-OH-DHP, may contribute to this adaptation of pregnancy.

Angiotensin II modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism in rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1009-R1016 ◽  
Author(s):  
Y. Nishida ◽  
K. L. Ryan ◽  
V. S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Before And After ◽  
Dose Dependent ◽  
Renal Sympathetic

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on baroreflex function curves before and after intravertebral administration of the alpha 1-adrenoreceptor antagonist prazosin. Rabbits were chronically instrumented with subclavian and vertebral arterial catheters, venous catheters, and aortic and vena caval occludes. Baroreflex curves were obtained by relating heart rate (HR) to mean arterial pressure during increases and decreases in arterial pressure. Intravertebral infusions of ANG II (5, 10, and 20 ng.kg-1.min-1) produced a dose-dependent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretreatment with prazosin (10 micrograms/kg) via the vertebral artery markedly reduced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II resets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha 1 mechanism. When the effects of vertebral ANG II on the baroreflex control of renal sympathetic nerve activity (RSNA) were examined, intravertebral administration of ANG II, while reducing the gain and the maximum RSNA, did not reset the RSNA baroreflex curve. These data suggest that ANG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha 1-adrenergic mechanism.

Effect of exercise training on RSNA, baroreflex control, and blood pressure responsiveness

1993 ◽  
Vol 265 (2) ◽  
pp. R365-R370 ◽  
Author(s):  
C. E. Negrao ◽  
M. C. Irigoyen ◽  
E. D. Moreira ◽  
P. C. Brum ◽  
P. M. Freire ◽  
...  
Keyword(s):  
Exercise Training ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Analog To Digital ◽  
Male Wistar Rats ◽  
Reflex Control ◽  
Renal Sympathetic

The effect of exercise training (ET) on renal sympathetic nerve activity (RSNA), baroreflex control of RSNA and heart rate (HR), and arterial pressure (AP) responsiveness to phenylephrine and angiotensin II (ANG II) was studied in six trained (T) and six sedentary (S) male Wistar rats. ET was performed on a motor treadmill for 13 wk. The RSNA signals of unanesthetized rats were processed by an analog-to-digital converter to quantify the nerve discharges associated with changes in AP and HR. The reflex control of RSNA and HR were evaluated during progressive injections of phenylephrine and sodium nitroprusside. Mean arterial pressure (MAP) was similar in both groups. RSNA was significantly lower in T rats (28 +/- 2 vs. 36 +/- 3%). T rats had an impairment of baroreflex control of RSNA in response to nitroprusside (4.9 +/- 0.89 vs. 12.3 +/- 1.2 bars.cycle-1.mmHg-1). ET decreased AP responsiveness for phenylephrine and ANG II. Therefore ET produces 1) no change in resting MAP but a significant decrease in RSNA and AP responsiveness and 2) partial impairment of baroreflexes, i.e., bradycardic responses and RSNA during MAP decrease.

Arginine vasopressin modulation of arterial baroreflex responses in fetal and newborn sheep

1996 ◽  
Vol 271 (6) ◽  
pp. R1643-R1653 ◽  
Author(s):  
A. M. Nuyt ◽  
J. L. Segar ◽  
A. T. Holley ◽  
M. S. O'Mara ◽  
M. W. Chapleau ◽  
...  
Keyword(s):  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Maximal Stimulation ◽  
Phenylephrine Infusion ◽  
Renal Sympathetic ◽  
Newborn Animals

The present study was designed to test the hypothesis that the influence of circulating vasopressin (AVP) on the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) changes during development. To test this hypothesis, we studied arterial baroreflex-mediated control of HR and RSNA in the presence of increasing plasma levels of AVP in conscious, chronically instrumented fetal, newborn, and adult sheep. In fetal and newborn sheep, increasing plasma AVP levels (from < 10 to > 200 microU/ml) increased resting levels of mean arterial blood pressure (MABP) and decreased HR and RSNA. HR and RSNA baroreflex responses to variations of MABP with nitroprusside and phenylephrine infusion were not modified by elevated AVP levels in either newborn or fetal sheep, except for a small decrease in maximal HR response to nitroprusside infusion in the newborn animals. In contrast, in adults, AVP caused bradycardia and a decrease in RSNA without change in MABP, accompanied by resetting of the arterial baroreflex (decrease in maximal HR and RSNA, decrease in RSNA gain, and shift of HR to lower pressure). To test the hypothesis that the inability of AVP to reset the arterial baroreflex early during development was not secondary to maximal stimulation of V1 receptors during baseline conditions, we investigated the effect of V1-receptor blockade on baseline cardiovascular and arterial baroreflex function in newborn lambs. Administration of a V1-receptor antagonist produced no significant changes in resting MABP, HR, and RSNA and did not influence arterial baroreflex-mediated changes in HR and RSNA. These results indicate that, contrary to adults, circulating AVP does not modulate the arterial baroreflex in fetal and newborn sheep.

Arterial baroreceptor reflex control of renal sympathetic nerve activity following chronic myocardial infarction in male, female, and ovariectomized female rats

2015 ◽  
Vol 309 (2) ◽  
pp. R169-R178 ◽  
Author(s):  
Maximilian I. Pinkham ◽  
Gillian A. Whalley ◽  
Sarah-Jane Guild ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett
Keyword(s):  
Myocardial Infarction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sham Group ◽  
Chronic Myocardial Infarction ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

There is controversy regarding whether the arterial baroreflex control of renal sympathetic nerve activity (SNA) in heart failure is altered. We investigated the impact of sex and ovarian hormones on changes in the arterial baroreflex control of renal SNA following a chronic myocardial infarction (MI). Renal SNA and arterial pressure were recorded in chloralose-urethane anesthetized male, female, and ovariectomized female (OVX) Wistar rats 6–7 wk postsham or MI surgery. Animals were grouped according to MI size (sham, small and large MI). Ovary-intact females had a lower mortality rate post-MI (24%) compared with both males (38%) and OVX (50%) ( P < 0.05). Males and OVX with large MI, but not small MI, displayed an impaired ability of the arterial baroreflex to inhibit renal SNA. As a result, the male large MI group (49 ± 6 vs. 84 ± 5% in male sham group) and OVX large MI group (37 ± 3 vs. 75 ± 5% in OVX sham group) displayed significantly reduced arterial baroreflex range of control of normalized renal SNA ( P < 0.05). In ovary-intact females, arterial baroreflex control of normalized renal SNA was unchanged regardless of MI size. In males and OVX there was a significant, positive correlation between left ventricle (LV) ejection fraction and arterial baroreflex range of control of normalized renal SNA, but not absolute renal SNA, that was not evident in ovary-intact females. The current findings demonstrate that the arterial baroreflex control of renal SNA post-MI is preserved in ovary-intact females, and the state of left ventricular dysfunction significantly impacts on the changes in the arterial baroreflex post-MI.

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