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Role of Vasopressin in Rat Models of Salt-Dependent Hypertension

  • Secondary Hypertension: Nervous System Mechanisms (M Wyss, Section Editor)
  • Published:
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Abstract

Purpose of Review

Dietary salt intake increases both plasma sodium and osmolality and therefore increases vasopressin (VP) release from the neurohypophysis. Although this effect could increase blood pressure by inducing fluid reabsorption and vasoconstriction, acute activation of arterial baroreceptors inhibits VP neurons via GABAA receptors to oppose high blood pressure. Here we review recent findings demonstrating that this protective mechanism fails during chronic high salt intake in rats.

Recent Findings

Two recent studies showed that chronic high sodium intake causes an increase in intracellular chloride concentration in VP neurons. This effect causes GABAA receptors to become excitatory and leads to the emergence of VP-dependent hypertension. One study showed that the increase in intracellular chloride was provoked by a decrease in the expression of the chloride exporter KCC2 mediated by local secretion of brain-derived neurotrophic factor and activation of TrkB receptors.

Summary

Prolonged high dietary salt intake can cause pathological plasticity in a central homeostatic circuit that controls VP secretion and thereby contribute to peripheral vasoconstriction and hypertension.

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Abbreviations

BDNF:

Brain-derived neurotrophic factor

DBB:

Diagonal band of Broca

GABA:

γ-Aminobutyric acid

KCC2:

K–Cl co-transporter type 2

MNCs:

Magnocellular neurosecretory cells

MNPO:

Median preoptic nucleus

NKCC1:

Na–Cl co-transporter type 1

NTS:

Nucleus of the solitary tract

OVLT:

Organum vasculosum laminae terminalis

PVN:

Paraventricular nucleus

SON:

Supraoptic nucleus

SFO:

Subfornical organ

TrkB:

Tropomyosin receptor kinase B

VP:

Vasopressin

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Acknowledgments

C.W.B. is recipient of a James McGill Research Chair. D.I.L. is recipient of a Canada Graduate Scholarship. This work was supported by grants to C.W.B. from the Heart and Stroke Foundation of Canada (G-16-00014197) and the Canadian Institutes of Health Research (FDN-143337) and by a John J. Day Legacy Award of Excellence to C.W.B. The Research Institute of the McGill University Health Center receives generous funding from the Fonds de Recherche du Québec Santé.

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This article is part of the Topical Collection on Secondary Hypertension: Nervous System Mechanisms

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Prager-Khoutorsky, M., Choe, K.Y., Levi, D.I. et al. Role of Vasopressin in Rat Models of Salt-Dependent Hypertension. Curr Hypertens Rep 19, 42 (2017). https://doi.org/10.1007/s11906-017-0741-2

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