Blood pressure and heart rate responses to microinjection of vasopressin into the nucleus tractus solitarius region of the rat

Matsuguchi, H; Sharabi, Fouad M.; Gordon, Frank J.; Johnson, Alan Kim; Schmid, Phillip G.

doi:10.1016/0028-3908(82)90012-0

Cited by 195 publications

(57 citation statements)

References 23 publications

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“…Norepinephrine, acetylcholine, epinephrine, Lglutamate, dopamjne, and other agents are known to reduce blood pressure and heart rate when injected into the NTS. In contrast, certain agents, such as angiotensin II, 26 vasopressin, 27 and yohimbine, 28 have been shown to raise blood pressure and heart rate when injected into this site.…”

Section: Discussionmentioning

confidence: 94%

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

et al. 1988

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SUMMARY Adenosine acts at many sites to modulate neuronal activity. The purpose of this study was to investigate a possible role for adenosine as a neuromodnlator of brainstem cardiovascular control. Microinjections of adenosine (0-2.3 nmol) were made stereotaxically into various brainstem sites. Injection of adenosine into the nucleus tractus solitarii (NTS) produced dose-related decreases in heart rate and systolic and diastolic blood pressures. Maximal changes occurred 90 seconds after injection. Injection into the area postrema also produced decreased heart rate and systolic and diastolic blood pressures. No significant effect occurred following injection into the Cl area. Adenosine 5-triphosphate and its analogue, /3,-y-methylene adenosine 5-triphosphate also produced doserelated and potent vasodepressor and bradycardia effects in the NTS. Injection of l,3-dipropyl-8-psulfophenylxanthine (0.92 nmol), a potent adenosine receptor antagonist, produced no effect itself, but abolished for 45 minutes the actions of further injections of adenosine and adenosine 5'-triphosphate (but not L-glutamate) in both the NTS and area postrema. Thus, NTS and area postrema injections of adenosine decrease blood pressure and heart rate in anesthetized normotensive rats through adenosine receptors located in these areas. These findings support a role for endogenous adenosine as a central modulator in cardiovascular control. (Hypertension 11: 191-197, 1988) KEY WORDS • adenosine • adenosine 5'-triphosphate • central nervous system • nucleus tractus solitarii • area postrema • rats • nucleosides • purines • purinergic neurotransmission A UTONOMIC cardiovascular control is achieved / \ in the medulla oblongata through integration X \ . of input from higher centers with afferent input from receptors in chest and neck structures.1 This afferent input travels in the vagus and glossopharyngeal nerves and terminates principally in the nucleus tractus solitarii (NTS). NTS neurons have projections to many rostral and ventral sites. The Cl area in the ventrolateral medulla, which contributes to the tonic control over sympathetic outflow, receives some of these NTS projections.2 Stimulation of the NTS produces inhibition of sympathetic tone, while stimulation of the Cl area leads to an increase in sympathetic activation.

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Section: Discussionmentioning

confidence: 94%

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

et al. 1988

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“…Several studies have demonstrated that AVP may influence the cardiovascular-related functions of the NTS, increasing arterial pressure, heart rate and circulating catecholamines, suggesting activation of the sympathetic nervous system. There is evidence that the increased release of AVP may enhance the sensitivity of some neurons to the same level of baroreceptor stimulation, increasing baroreflex sensitivity [55][56][57].…”

Section: Discussionmentioning

confidence: 99%

Availability of a rich source of sodium during the perinatal period programs the fluid balance restoration pattern in adult offspring

Macchione

Caeiro

Godino

et al. 2012

Physiology & Behavior

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“…22 ' 7S ' M Thus, any role for these actions of VP in modulating the hypertensive process in SHR should have been blocked in the antagonist-infused animals in the current study. Specifically, renin secretion is inhibited by VP, 28 but this effect is reversed in the presence of d(CH 2 ) 3 Tyr(Me)AVP.…”

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confidence: 92%

“…39 Thus, it is possible that the chronic infusion of d(CH 2 ) 3 Tyr(Me)AVP attenuated the secretion of atrial natriuretic factor as well as blocked the vasoconstrictor actions of VP and, therefore, would simultaneously have removed offsetting pressor and depressor influences, resulting in no net change in the hypertensive process. Finally, the ability of VP to increase heart rate and blood pressure when injected either into the cerebral ventricles or into the nucleus of the tractus solitarius or the locus ceruleus is blocked by central administration of d(CH 2 ) J Tyr(Me)AVP 22 ' 3M4 but not by acute intravenous administration. 40 Thus, it is possible that this site of action of VP was not blocked in the current study, although under conditions of chronic infusion, the V, antagonist may gain access to the central nervous system.…”

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confidence: 97%

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Evidence against a pressor role for vasopressin in spontaneous hypertension.

Sladek¹,

Blair²,

Mangiapane³

1987

Hypertension

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Received May 12, 1986; accepted October 6, 1986. to WKY, 1 ' 2 and at 5 and 8 weeks of age VP release is exaggerated in SHR relative to WKY in response to a decrease in plasma volume in vivo 3 or following exposure of the hypothalamoneurohypophyseal system to acetylcholine and angiotensin II in vitro. 4 ' 5 Thus, increased secretion of VP in response to selected stimuli may underlie the elevation of plasma and urinary VP in SHR.Peripheral resistance is elevated in SHR, 6 ' 7 and this elevation is thought to be central to the hypertensive process. Although increased activity of the sympathetic nervous system in SHR' represents one mechanism contributing to the elevated peripheral resistance, VP may also contribute to the elevation of peripheral resistance in this model of hypertension. In addition to the elevations in circulating VP already mentioned, the pressor potency of VP is greater in SHR than in WKY.9 -I0 The pressor potency of VP in SHR appears to stem from impairment of the baroreceptor reflexes that buffer against the pressor effects of VP in WKY.10 '" These observations, in conjunction with the

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Blood pressure and heart rate responses to microinjection of vasopressin into the nucleus tractus solitarius region of the rat

Cited by 195 publications

References 23 publications

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

Availability of a rich source of sodium during the perinatal period programs the fluid balance restoration pattern in adult offspring

Evidence against a pressor role for vasopressin in spontaneous hypertension.

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