Changes in cerebrospinal fluid Na+ concentration do not underlie hypertensive responses to dietary NaCl in spontaneously hypertensive rats

doi:10.1016/0006-8993(90)91212-Y

Brain Research

Volume 506, Issue 1, 1 January 1990, Pages 149-152

https://doi.org/10.1016/0006-8993(90)91212-Y Get rights and content

Abstract

This study tests the hypothesis that dietary NaCl loading increases cerebrospinal fluid (CSF) Na⁺ concentration in NaCl-sensitive spontaneously hypertensive rats (SHR-S), resulting in an increase in arterial pressure. The high NaCl diet caused a significant rise in systolic arterial pressure in SHR-S but not in normotensive Wistar Kyoto (WKY) rats. In contrast, the high NaCl diet caused a transient rise in CSF Na⁺ that was similar in amplitude in SHR-S and WKY. A second experiment demonstrated that in SHR-S, concomitant dietary Ca²⁺ supplementation attenuated the dietary NaCl-induced exacerbation of hypertension, but did not alter the transient increase in CSF Na⁺ concentration. Together, these results indicate that alterations in CSF Na⁺ concentration do not contribute to the increase in arterial pressure induced by a high NaCl diet in SHR-S.

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The central and peripheral nervous system is typically considered to be a short-term modifier of sympathetic nervous system activity, but several lines of evidence suggest that they contribute to chronic elevation of arterial pressure in at least some forms of hypertension. Our studies focus on the mechanisms underlying NaCl-sensitive hypertension in the spontaneously hypertensive rat (SHR). When these rats are fed a high NaCl diet, their arterial pressure rapidly increases and is maintained about 30 mm Hg higher than those of pair fed controls. The increase in arterial pressure is associated with a decrease in norepinephrine release, specifically in the anterior hypothalamic nucleus (AHN), resulting in increased sympathetic nervous system activity, peripheral vasoconstriction, and arterial pressure. Furthermore, administration of an α₂-adrenergic receptor agonist in this area blocks the NaCl-sensitive increase in arterial pressure in the SHR but has no significant effect on arterial pressure in normotensive controls. We have identified three intermediary steps by which dietary NaCl reduces AHN norepinephrine release. First, dietary NaCl causes an increase in plasma NaCl and a blunting of the plasma NaCl circadian rhythm. Second, alterations in plasma NaCl activate osmosensitive neurons in the organum vasculosum of the lamina terminalis (OVLT). Third, OVLT input to the AHN appears to increase the release of atrial natriuretic peptide with a resultant decrease in the local release of norepinephrine. Finally, our evidence demonstrates that these factors lead to an increased rise in sympathetic nervous system activity during the early wake phase in SHR on a high NaCl diet, contributing to NaCl-sensitive hypertension in SHR.
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The contribution of the central interaction between calcium and sodium to hemodynamic regulation was assessed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. The effect of a high calcium solution (Ca²⁺, 130 mg/dl, 10 μl) infused into the cerebral ventricle (i.c.v.) on hemodynamic responses induced by a high sodium solution (Na⁺, 1,000 mEq/l, 10 μl) i.c.v. and the mechanism by which high Ca²⁺ affects the hemodynamic responses induced by high Na⁺ i.c.v. were studied. High Na⁺ i.c.v. induced a pressor response with tachycardia in the SHRs, but induced a pressor response with reflex bradycardia in the WKYs. Prior treatment with high Ca²⁺ i.c.v. attenuated the pressor response induced by high Na⁺ i.c.v. (+55.6 ± 4.4 to 33.1 ± 3.2 mmHg, P < 0.01) and restored reflex bradycardia (+86.4 ± 7.7 to −26.7 ± 7.6 bpm, P < 0.01) in SHRs. Whereas prior treatment with high Ca²⁺ i.c.v. attenuated the pressor response (+35.7 ±2.0 to +22.2 ± 4.0 mmHg, P < 0.05), it did not alter the degree of reflex bradycardia (−81.7 ± 7.1 to −69.2 ± 120 bpm, n.s.) in WKYs. Ganglionic blockade attenuated the pressor response (56.9 ± 3.5 to 42.9 ± 2.3 mmHg, P < 0.05) and restored reflex bradycardia (+82.1 ± 10.3 to −65.9 ± 11.0 bpm, P < 0.01) in SHRs, whereas, inhibition of arginine vasopressin attenuated the pressor response without modification of the tachycardic response. These results suggest (i) that central Ca²⁺ antagonizes the pressor response to central Na⁺ by inhibiting sympathetic nervous system activity and (ii) that central Ca²⁺ functions in the regulation of baroreflex control of the heart rate in SHRs. Central Ca²⁺ may have importance in cardiovascular regulation of hypertension.
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: This work was supported in part by National Heart, Lung and Blood Institutes Grants HL 37722, HL 22544, HL 25452, HL 36390, HL 35051, and by a grant from the National Dairy Board and administered in cooperation with National Dairy Council.

^*: Present address: Department of Biochemistry, Khon Kaen University, Khon Kaen, Thailand.

View full text

Changes in cerebrospinal fluid Na+ concentration do not underlie hypertensive responses to dietary NaCl in spontaneously hypertensive rats

Abstract

Physiol. Behav.

Brain Research

Brain Research

Brain Research

Brain Research

Preoptic-hypothalamic periventricular lesions: thirst deficits and hypernatremia

Am. J. Physiol.

Sympathetic hyperactivity elevates blood pressure during acute cerebroventricular infusions of hypertonic salt in rats

J. Cardiovas. Pharmacol.

High NaCl diet reduces hypothalamic norepinephrine turnover in hypertensive rats

Hypertension

How does salt raise blood pressure?

Hypertension

Ionic modulation of alpha-adrenoceptors

J. Cardiovas. Pharmacol.

Alterations in cerebrospinal fluid sodium and osmolality in rats during one-kidney, one-wrap renal hypertension

Clin. Exp. Pharmacol. Physiol.

Changes in cerebrospinal fluid Na⁺ concentration do not underlie hypertensive responses to dietary NaCl in spontaneously hypertensive rats