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.

Brain angiotensin II tonically modulates sympathetic baroreflex in rabbit ventrolateral medulla

1996 ◽  
Vol 271 (3) ◽  
pp. H1015-H1021 ◽  
Author(s):  
T. Saigusa ◽  
M. Iriki ◽  
J. Arita
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Renal Sympathetic

The role of endogenous angiotensin II (ANG II) at the level of the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in the control of sympathetic baroreflex function was investigated in urethan-anesthetized rabbits. The baroreflex relationship between mean arterial pressure and integrated renal sympathetic nerve activity (RSNA) was compared before and during microinfusion of saralasin, an ANG II receptor antagonist into RVLM or CVLM. The infusion of saralasin (20 pmol/min) into RVLM reduced the upper plateau, the range, and the range-dependent gain of the baroreflex, as well as the resting level of RSNA. The infusion of saralasin into CVLM augmented the upper plateau, the reflex range, and the range-dependent gain, whereas it did not alter the resting level of RSNA or mean arterial pressure. These results suggest that 1) the ANG II networks in RVLM are tonically active, influencing the resting level of the sympathetic outflow and facilitating the sympathetic baroreflex function, and 2) the ANG II networks in CVLM do not significantly influence the sympathetic activity in the resting state but exert an inhibitory effect on the baroreflex response when arterial pressure falls below the resting level.

α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

2002 ◽  
Vol 282 (6) ◽  
pp. H2336-H2345 ◽  
Author(s):  
Linda F. Hayward ◽  
Alecia P. Riley ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Baroreflex Function ◽  
Wistar Kyoto ◽  
Renal Sympathetic

We examined the effect of α2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered α2-adrenoreceptor mechanisms in SHR.

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.

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.

Role of endogenous angiotensin II on sympathetic reflexes in conscious rabbits

1997 ◽  
Vol 272 (6) ◽  
pp. R1816-R1825 ◽  
Author(s):  
R. D. Bendle ◽  
S. C. Malpas ◽  
G. A. Head
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Ang Ii ◽  
At1 Antagonist ◽  
Before And After ◽  
Sympathetic Reflexes ◽  
Conscious Rabbits ◽  
Dose Dependent ◽  
Renal Sympathetic

In the present study we sought to determine the contribution of endogenous brain stem angiotensin to renal sympathetic reflexes in conscious rabbits. Initial studies determined the subtype of receptor involved in the pressor response to angiotensin II (ANG II) administration into the fourth ventricle (4V). The AT1 antagonist losartan (0.001-10 micrograms 4V) had no effect on blood pressure alone but caused a dose-dependent blockade of the pressor effect of ANG II, with complete blockade produced by 10 micrograms, an effect that lasted for at least 3 h. The AT2 antagonist PD-123319 (0.1-1,000 micrograms) and vehicle had no effect on the ANG II pressor response. The effect of losartan (10 micrograms) on the baroreceptor, chemoreceptor, and trigeminal reflexes was examined in eight rabbits that had been implanted with 4V catheters and an electrode for recording renal sympathetic nerve activity (RSNA) 1 wk earlier. Baroreflex assessments were made during normoxia and two conditions of hypoxia (10% O2 and 10% O2 + 3% CO2) before and after 10 micrograms losartan or vehicle, on separate experimental days. During normoxia and hypoxia+CO2 losartan increased resting RSNA, the range, and upper plateau of the RSNA-MAP baroreflex curves. By contrast the marked increase in RSNA due to activation of trigeminal afferents was not affected by losartan. In conclusion the effect of losartan to increase RSNA activity in conscious rabbits, particularly during hypoxia and baroreceptor unloading, suggests that endogenous ANG II via AT1 receptors normally inhibits renal sympathetic baroreceptor and chemoreceptor reflexes.

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

1984 ◽  
Vol 246 (1) ◽  
pp. H80-H89 ◽  
Author(s):  
G. B. Guo ◽  
F. M. Abboud
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Reflex Inhibition ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Excitatory Effect ◽  
Baroreflex Control ◽  
Reflex Bradycardia ◽  
Background Infusion

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

scholarly journals Nitric oxide and angiotensin II regulate cardiovascular homeostasis and the arterial baroreflex control of heart rate in conscious lambs

2011 ◽  
Vol 13 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Stephanie J Wehlage ◽  
Francine G Smith
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Before And After ◽  
Cardiovascular Homeostasis ◽  
New Evidence

To investigate the potential role of angiotensin II (Ang II) type 1 receptors (AT1Rs) as well as endogenously produced nitric oxide (NO) in regulating cardiovascular homeostasis during ontogeny, experiments were carried out in conscious lambs aged approximately 1 week ( N = 9) and 6 weeks ( N = 11). The arterial baroreflex control of heart rate (HR) was assessed before and after intravenous (IV) infusion of the selective AT1R antagonist, ZD 7155, before and after IV administration of the L-arginine analogue, NG-nitro-L-arginine methyl ester (L-NAME). In both groups, after ZD 7155 alone, mean arterial pressure decreased then increased after L-NAME. At 1 but not 6 weeks, HR decreased after ZD 7155 as well as after L-NAME. At 1 but not 6 weeks, there was a decrease in the HR range after ZD 7155 and after ZD 7155 + L-NAME, as compared to control. There was also a decrease in minimum HR after ZD 7155 + L-NAME at 1 week. These data provide new evidence that, together, Ang II and NO regulate cardiovascular homeostasis as well as the arterial baroreflex of HR early in life which may help to explain the activation of these two systems early in life.

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.

Central effect of angiotensin II on baroreflex regulation in conscious rabbits

1989 ◽  
Vol 256 (3) ◽  
pp. R694-R700 ◽  
Author(s):  
Y. Matsumura ◽  
E. M. Hasser ◽  
V. S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Vena Cava ◽  
Reflex Inhibition ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Intravenous Infusions ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Central effects of angiotensin II (ANG II) on arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) were examined in conscious rabbits. Intravenous infusions of ANG II (5-320 ng.kg-1.min-1) significantly reduced the baroreflex inhibition of HR compared with phenylephrine (PE) (0.5-16 micrograms.kg-1.min-1), whereas reflex inhibition of RSNA was unaltered. Background intravenous infusions of ANG II did not alter the baroreflex responses of RSNA nor HR to increases (with PE) or decreases in mean arterial pressure (with nitroglycerin or inferior vena cava occluder). When ANG II was infused into the vertebral artery (VA) the integrated pressor response was greater than intravenous infusions. Progressive VA infusions of ANG II resulted in a significantly blunted baroreflex inhibition of HR compared with intravenous infusions, whereas the reflex inhibition of RSNA was identical between VA and intravenous infusions. These results suggest that ANG II produces central pressor effects via a hindbrain site and reduces baroreflex inhibition of HR without altering baroreflex inhibition of RSNA.

ANG II and baroreflex function in rabbits with CHF and lesions of the area postrema

1999 ◽  
Vol 277 (1) ◽  
pp. H342-H350 ◽  
Author(s):  
Jun-Li Liu ◽  
Hiroshi Murakami ◽  
Max Sanderford ◽  
Vernon S. Bishop ◽  
Irving H. Zucker
Keyword(s):  
Baroreflex Sensitivity ◽  
Area Postrema ◽  
Venous Pressure ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
New Zealand White Rabbits ◽  
Before And After ◽  
Renal Sympathetic

Blockade of the angiotensin II (ANG II) type 1 receptor (AT1) has been shown to restore baroreflex sensitivity in rats and rabbits with experimental chronic heart failure (CHF). Because the modulation of baroreflex function in response to ANG II is mediated in part by AT1 receptors located in the area postrema, we hypothesized that lesions of the area postrema would prevent the enhancement in baroreflex function in response to AT1-receptor blockade in rabbits with pacing-induced CHF. Experiments were carried out on 24 male New Zealand White rabbits that were divided into sham ( n = 12) and lesioned ( n = 12) groups further divided into normal and CHF subgroups ( n = 6 each). All rabbits were identically instrumented to measure cardiac external dimensions, central venous pressure, arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA). After 3–4 wk of pacing, baroreflex sensitivity (infusions of phenylephrine and nitroprusside) was evaluated before and after intravenous administration of the AT1-receptor antagonist L-158,809. Maximum baroreflex sensitivity in nonpaced rabbits was 5.4 ± 0.7 beats ⋅ min−1 ⋅ mmHg−1and 5.2 ± 0.5% of maximum/mmHg for HR and RSNA curves, respectively, and was not altered by L-158,809 in either intact or lesioned rabbits. In contrast, L-158,809 enhanced baroreflex sensitivity in intact rabbits with CHF (HR from 1.6 ± 0.3 to 4.1 ± 0.7 beats ⋅ min−1 ⋅ mmHg−1, P < 0.001; RSNA from 2.3 ± 0.2 to 4.9 ± 0.4% of maximum/mmHg, P < 0.001). However, in CHF rabbits with area postrema lesions, L-158,809 failed to enhance baroreflex sensitivity. Interestingly, area postrema lesions did not normalize the baroreflex in CHF rabbits. From these data we conclude that the area postrema mediates the normalization of baroreflex sensitivity after AT1 blockade in rabbits with CHF but does not modify resting baroreflex function.

Sign in / Sign up

Export Citation Format

Share Document