Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

Abstract

To investigate the effects of antihypertensive treatment with four currently used agents (trichlormethiazide, atenolol, nicardipine, and enalapril) on the arterial baroreceptor function at the early phase of hypertension, we administered the agents to spontaneously hypertensive rats and WistarKyoto rats from 8 to 10 weeks of age and examined the aortic nerve activity function. In untreated spontaneously hypertensive rats, the relation between the arterial pressure and aortic nerve activity was shifted to the right, that is, to a higher pressure level (threshold pressure, 90±3 versus 76±1 mm Hg, P<.05), and the maximum gain which was obtained by logistic function analysis was depressed (1.55±0.08% versus 2.18±0.13% maximum/mm Hg, f<.01) as compared with untreated Wistar-Kyoto rats. An equivalent decrease in arterial pressure with each of the four agents (-20±l mm Hg, P<.01) B aroreceptor activity transmitted to the central nervous system (CNS) is a primary signal concerning moment-to-moment alterations in arterial pressure and represents a fundamental mechanism in the neural control of the circulation because it triggers reflex inhibition of sympathetic nerve activity and excitation of parasympathetic nerve activity that buffers the rise in pressure. It is known that the baroreceptor function is depressed in several forms of hypertension. 1 " 3 Impaired baroreceptor input to the CNS elicits instability of the circulation, 4 which tends in turn to lead to increases in cardiovascular morbidity and mortality. Agents that effectively potentiate the baroreceptor function are considered preferable in the treatment of hypertension. Early studies have shown that conventional antihypertensive therapy with combinations of drugs (diuretics, vasodilators, and adrenergic antagonists) increased the baroreceptor sensitivity in spontaneously hypertensive rats (SHRs). classes of antihypertensive agents might exert distinct effects on the baroreceptor function through specific pharmacological actions when administered chronically to hypertensive subjects. To test this hypothesis, we treated SHRs with one of four currently used agents (a diuretic, a j3-adrenergic blocker, a calcium channel blocker, and an ACE inhibitor) for 2 weeks and examined the effects on the aortic baroreceptor function. Moreover, we used relatively young SHRs (10 weeks of age) in which the characteristics of the aorta are less damaged by hypertension 3

Rostral Ventrolateral Medulla Neurons of Neonatal Wistar-Kyoto and Spontaneously Hypertensive Rats

“…[1][2][3] We have reported impairment of the baroreflex function in hypertension based on recordings of renal SNA (RSNA) in conscious rabbits and rats and on vagal afferent nerve activity. 4,5 We have also confirmed that the angiotensin (Ang) II type 1 (AT 1 ) receptor antagonist candesartan improves the impaired baroreflex in conscious rats with congestive heart failure. 6 Earlier studies examined the responses of BP and SNA to Ang II and Ang II antagonists microinjected into the RVLM of normotensive and hypertensive animals, [7][8][9][10][11] because the RVLM area contains Ang II-immunoreactive nerve terminals and a moderately high density of AT 1 receptors.…”

Elevated Fos Expression in the Nucleus Tractus Solitarii Is Associated With Reduced Baroreflex Response in Spontaneously Hypertensive Rats

“…Two studies 30,31 in which antihypertensive agents were used to treat hypertension indicate that reduction in SAP by itself may directly potentiate the function of BRR. As such, it is possible that restoration of BRR sensitivity by ASON1 in SHR and SHRSP may result from the depressor effect of this antisense oligonucleotide.…”

Effects of spaceflight on postnatal development of arterial baroreceptor reflex in rats

“…The electrical activity was amplified using an amplifier (AB-651J, Nihon Kohden) with a band pass filter of 50-3000 Hz. The amplified activity was rectified and integrated using an integrator (EI-601GS, Nihon Kohden) with a 2 s time constant (Ichikawa et al 1994, Waki et al 1997. MBP was raised by 30-50 mmHg by a bolus injection of phenylephrine (20-50 lg kg )1 ).…”