Cardiovascular Neurons In Rostral Ventrolateral Medulla Research Articles

Effects of Angiotensin II on the Spontaneous Activity of Rostral Ventrolateral Medullary Cardiovascular Neurons and Blood Pressure in Spontaneously Hypertensive Rats.

The interactive role of rostral ventrolateral medulla (RVL) cardiovascular neurons and brain angiotensin II (Ang II) in regulating the arterial blood pressure was examined by recording simultaneously the spontaneous activity of these spinal projecting neurons and the arterial blood pressure in the pentobarbital-anesthetized spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar Kyoto rat (WKY). It was found that Ang II elicited dose-dependent excitatory responses in a subpopulation of RVL cardiovascular neurons, followed by a subsequent increase in blood pressure. These effects of Ang II were significantly greater in SHR than in WKY. The effects were attenuated or abolished by co-administration of Ang II antagonist, [Sar(1), Ile(8)]-Ang II to RVL using bilateral microinjection attenuated the blood pressure effects of intracerebroventricularly administered Ang II by as much as 70%. These results indicated that spinal projecting RVL cardiovascular neurons are important in mediating the pressor action of Ang II. The enhanced sensitivity and responsiveness of RVL cardiovascular neurons to Ang II may be pertinent to the genesis of hypertension in adult SHR. Copyright 1996 S. Karger AG, Basel

Effects of [sar 1, Ile 8]-angiotensin II on rostral ventrolateral medulla neurons and blood pressure in spontaneously hypertensive rats

The present study was an attempt to determine the influence of brain angiotensin II, the activity of which is known to be higher in spontaneously hypertensive rat, on the spontaneous activity of the cardiovascular neurons in the rostral ventrolateral medulla of the spontaneously hypertensive rat. Both the spontaneous activity of the spinal projecting rostral ventrolateral medulla cardiovascular neurons and the arterial blood pressure were simultaneously measured in the pentobarbital-anesthetized spontaneously hypertensive rat and its normotensive control, the Wistar Kyoto rat, following microinjection to rostral ventrolateral medulla of an angiotensin II antagonist, [Sar 1, Ile 8]-angiotensin II (sarile). A microinjection method was developed that enabled us to perform extracellular recording of the rostral ventrolateral medulla cardiovascular neuron during the microinjection of drug to the vicinity of the neuron. It was found that sarile reduced both the arterial blood pressure and firing rate of some rostral ventrolateral medulla cardiovascular neurons dose-dependently. The effects of sarile were significantly greater in spontaneously hypertensive rat than in the Wistar Kyoto rat. The present findings indicate that the rostral ventrolateral medulla cardiovascular neurons of spontaneously hypertensive rat exhibit an augmented sensitivity to endogenous brain angiotensin II. Such an increase in sensitivity to brain angiotensin II in the spontaneously hypertensive rat may contribute to the enhanced spontaneous activities of rostral ventrolateral medulla cardiovascular neurons, as in the sarile responsive single discharge units, even in the resting or prestimulation state. This interaction of brain angiotensin II and rostral ventrolateral medulla cardiovascular neurons is likely to be contributory to the genesis of hypertension in this strain of rats.

Somatic and visceral inputs to neurons of the rostral ventrolateral medulla

Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play an essential role in the generation of basal sympathetic tone and in the reflex regulation of blood pressure. In this study responses of RVLM "cardiovascular" neurons to somatic and visceral afferent stimulation were investigated. The activity of 34 RVLM neurons was recorded in urethan-anesthetized paralyzed and artificially ventilated rats. These neurons were identified as cardiovascular based on their baroreceptor sensitivity and their pulse-synchronous discharge. Electrical stimulation of the sciatic nerve excited 31 of the 34 RVLM units (91%). Renal nerve stimulation inhibited firing of 14 of 22 RVLM neurons tested (64%), not affecting the remaining 8 units. Stimulation of splenic nerves inhibited the discharge of 7 of 12 RVLM neurons tested (58%), whereas the remaining 5 units were not affected. All RVLM units responsive to visceral afferent stimulation were also responsive to sciatic nerve stimulation. These results indicate that RVLM cardiovascular neurons receive somatic and visceral inputs, suggesting an involvement of these units in the integration of homeostatic responses to changes in the internal and external environment.

Effects of chronic captopril treatment on the electrical-microstimulation-induced blood pressure changes and electrophysiological properties of cardiovascular neurons in the rostral ventrolateral medulla of the spontaneously hypertensive rat.

The effects of chronic treatment with captopril, an angiotensin-converting enzyme inhibitor, on various properties of the rostral ventrolateral medulla (RVL) were studied in spontaneous hypertensive rats (SHR) given captopril (orally at a dose of 30 mg/kg) or vehicle from the age of 4-5 weeks to 19-20 weeks. In SHR, such a treatment with captopril resulted in an arterial blood pressure similar to that of normotensive Wistar Kyoto rats (WKY). Upon electrical microstimulation of the RVL, the minimal threshold current required to elicit a pressor response in captopril-treated SHR was significantly higher than that observed in SHR. Furthermore, analysis of the discharge pattern of RVL spinal projecting cardiovascular neurons showed a significant difference between captopril-treated and untreated SHR with respect to the proportion of double discharge units and the regularity of single discharge units. These properties of the RVL in captopril-treated SHR were, however, similar to those of WKY. Upon withdrawal of electrical microstimulation, the secondary sustained pressor response characteristic of SHR, but not of WKY, persisted in captopril-treated SHR at a smaller magnitude and a shorter duration. These results indicate that the normalization of arterial blood pressure in SHR upon chronic oral treatment with angiotensin-converting enzyme inhibitor is associated with changes in properties of RVL cardiovascular neurons towards those of WKY. This suggests that brain angiotensin and RVL cardiovascular neurons play interactive roles in the development of hypertension in SHR.

Responses of cardiovascular neurons in the rostral ventrolateral medulla of the normotensive Wistar Kyoto and spontaneously hypertensive rats to iontophoretic application of angiotensin II

In female pentobarbital-anesthetized Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), changes in spontaneous discharges of cardiovascular neurons in the rostral ventrolateral medulla (RVL) in response to iontophoretic application of angiotensin II (Ang II) were studied and compared. It was found that iontophoretic application of Ang II to RVL increased the spontaneous neuronal activities of 30% of the cardiovascular neurons in both types of rats and that the increase was significantly greater in SHR than in WKY. In both types of rats, there was an increase in arterial blood pressure in response to iontophoretic release of Ang II to RVL. The pressor response was accompanied by tachycardia, which was significantly greater in SHR than in WKY. The present study provides evidence that Ang II acts directly on cardiovascular neurons in RVL, and in SHR, an enhanced sensitivity and responsiveness of the RVL cardiovascular neurons to Ang II may augment the sympathetic outflow from RVL and contribute to the genesis of hypertension.