Baroreflex control of renal sympathetic nerve activity is potentiated at early phase of two-kidney, one-clip Goldblatt hypertension in conscious rabbits.

Abstract

Conscious normotensive and two-kidney, one-clip Goldblatt hypertensive rabbits were studied to determine the sensitivity of the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate. The relations of the mean arterial pressure-RSNA and mean arterial pressure-heart rate were examined over a wide range of blood pressures produced by infusions of phenylephrine and nitroglycerin. The maximum slope obtained by logistic function analysis was considered to represent the baroreflex sensitivity. In the early hypertensive group (n=8; mean arterial pressure+SEM, 88±2 mm Hg) on day 5 after renal clip application, the maximum slope of the mean arterial pressure-RSNA relation was -11.3+± 1.2, which was significantly greater than that of the sham normotensive group (-6.9+±0.3, p<0.05). The maximum slope (-4.3+±0.2) of the mean arterial pressure-RSNA relation in the late hypertensive group (n=8; mean arterial pressure, 96±3 mm Hg) on day 21 after renal clipping was significantly smaller than that of another sham group (-7.2 +0.2, p <0.05). In contrast to these changes in the baroreflex control of RSNA, the control of heart rate was attenuated according to the magnitude of mean arterial pressure. To elucidate the mechanisms underlying the potentiated baroreflex, the effects of endogenous neuropeptides were investigated. First, plasma concentrations of angiotensin II and arginine vasopressin that are known to affect the baroreflex were determined. Plasma concentrations of vasopressin (3.1±0.6 pg/ml) as well as of angiotensin II (34±+7 pg/ml) were increased in the early hypertensive group, and the plasma vasopressin returned to a similar level to the sham group in the late hypertensive group (1.3+±0.4 pg/ml). Second, to study endogenous effects of these neuropeptides on the baroreflex, the maximum slopes of the baroreflex curves during infusions of antagonists for the peptides were determined in the early hypertensive group. The maximum slope of mean arterial pressure-RSNA during intravertebral arterial [Sar', Ala8]-angiotensin II (-16.4±1.5) was significantly greater (p<0.05), whereas the maximum slope during intravertebral arterial infusion of d(CH2)5Tyr(Me)arginine vasopressin (-4.7±0.5) was significantly smaller (p<0.05) than that during vehicle infusion (-11.3+±1.2). These results suggest that the baroreflex control of RSNA was potentiated in the early phase of two-kidney, one-clip hypertension in conscious rabbits and that endogenous arginine vasopressin and angiotensin II, which counteract each other, were apparently involved in the potentiated baroreflex mechanism. (Circulation Research 1990;67:1309-1322 H _~umoral factors such as angiotensin II (Ang hypertension.1-4 In addition to their actions on the II), arginine vasopressin (AVP), and norheart, the kidneys, and the blood vessels, these epinephrine (NE) are known to be involved peptides (Ang II and AVP) have been shown to in the development and maintenance of renovascular modulate the arterial baroreceptor reflex through various mechanis...

Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

“…1 In conscious rabbits with Ang II-dependent hypertension, the Ang II receptor antagonist [Sar 1 , Ala^Ang II not only reversed the high blood pressure but increased the maximum gain of the baroreceptor reflex control of renal sympathetic nerve activity (RSNA). 3 These data support the hypothesis that the antihypertensive effects of angiotensin converting enzyme (ACE) inhibitors are in part due to a centrally mediated decrease in sympathetic outflow. Because there are no in vivo studies on the Ang II receptor subtype that is functionally involved in the baroreceptor reflex, we compared the effects of angiotensin type 1 (AT^ and type 2 (AT 2 ) receptor antagonists on the baroreceptor reflex control of RSNA and heart rate (HR) in conscious spontaneously hypertensive rats (SHRs).…”

“…II-dependent hypertensive rabbits. 3 We have recently demonstrated that the baroreceptor reflex control of RSNA and HR is blunted in conscious SHRs compared with age-matched Wistar-Kyoto rats. 8 Moreover, in the latter study, 8 long-term treatment with lisinopril substantially enhanced the maximum gain of the baroreceptor reflex in SHRs.…”

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

“…Sustained decreases in A ltered central sympathetic outflow and decreased reflex control of peripheral sympathetic nerves are thought to be associated with established hypertension 14 ; however, the distinction between cause and effect is unclear. 5 - 6 The sympathetic nervous system could influence blood pressure control not only by its effect on the regulation of peripheral resistance but also by controlling volume homeostasis via efferent renal sympathetic nerve activity (RSNA). 7 -8 It is well established that RSNA influences tubular water and sodium reabsorption independent of changes in intrarenal and systemic hemodynamics.…”

“…- 6 The sympathetic nervous system could influence blood pressure control not only by its effect on the regulation of peripheral resistance but also by controlling volume homeostasis via efferent renal sympathetic nerve activity (RSNA).…”

Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II

“…In the first, the baroreflex curve is shifted or reset to a higher pressure, whereas in the second there is a decreased sensitivity of the reflex as measured by a decreased slope (or attenuated gain) of the baroreflex curve. These mechanisms have been documented in many experimental animal models of hypertension (10,17,25,26).…”