Handling of a Salt Load by Hypertensive and Normotensive Rats on Normal and Low Intakes of Sodium

Jm, Ledingham; Fo, Simpson

doi:10.1097/00004872-198404000-00007

Cited by 6 publications

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“…14,15 SHRs (stroke-prone spontaneously hypertensive rats) have normal extracellular fluid volumes and become hypertensive on salt loading, 16,17 whereas New Zealand genetically hypertensive (NZGH) rats have reduced extracellular fluid volumes and are insensitive to salt loading. 18,19 When crossed with Brattleboro rats, vasopressin-deficient SHR developed full hypertension, 14 whereas the blood pressures of vasopressin-deficient NZGH rats were lower than those of the original NZGH strain. 15 It seems that the blood pressure phenotype of V1aR À/À mice is more similar to that of NZGH than to that of SHR, because AVP action is indispensable for the basal blood pressure seen in V1aR À/À mice, as it is for the hypertensive response seen in NZGH rats.…”

Section: Decreased Sympathetic Nerve Activity In Central Nervous Systemmentioning

confidence: 99%

Vasopressin regulation of blood pressure and volume: findings from V1a receptor–deficient mice

Aoyagi

Koshimizu

Tanoue

2009

Kidney International

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[Arg(8)]-vasopressin (AVP) has several functions via its three distinct receptors, V1a, V1b, and V2. The V1a vasopressin receptor (V1aR) is expressed in blood vessels and involved in vascular contraction. Recently, we generated V1a receptor-deficient (V1aR(-/-)) mice and found that they were hypotensive. In addition, V1aR(-/-) mice exhibited (1) blunted AVP-induced vasopressor response, (2) impaired arterial baroreceptor reflex, (3) decreased sympathetic nerve activity, and (4) decreased blood volume, all of which could contribute to the observed hypotension. In relation to their decreased blood volume, V1aR(-/-) mice had decreased plasma aldosterone levels, which could result not only from decreased activity of the renin-angiotensin system (RAS), but also from impaired AVP-stimulated aldosterone release in the adrenal glands. V1aR was found to specifically co-express at the macula densa cells with cyclooxygenase (COX)-2 and with neuronal nitric oxide synthase, which produces potent stimulators of renin, PGE(2), and NO. The expression levels of renin, COX-2, and nNOS were significantly decreased in V1aR(-/-) mice, which led to the suppression of RAS activity and consequent decreases in aldosterone and blood volume. Furthermore, V1aR is also expressed in collecting duct cells and involved in regulating water reabsorption by affecting V2/aquaporin 2 function. Thus, AVP regulates blood pressure and volume via V1aR by exerting diverse functions in vivo.

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Section: Decreased Sympathetic Nerve Activity In Central Nervous Systemmentioning

confidence: 99%

Vasopressin regulation of blood pressure and volume: findings from V1a receptor–deficient mice

Aoyagi

Koshimizu

Tanoue

2009

Kidney International

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Vascular atrial natriuretic factor receptors in spontaneously hypertensive rats

Schiffrin

Parent

Louis

et al. 1992

Cardiovascular Research

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Sodium appetite as well as 24‐h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets

Ely

Thorén

Wiegand

et al. 1987

Acta Physiologica Scandinavica

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Young SHR and WKY rats were compared, first, concerning sodium (Na) appetite during 'rest', mild social stress and ACTH injections, second, concerning the diurnal patterns of water intake, urine output, mean arterial pressure (MAP) and heart rate (HR) while on various Na diets: 0.5 mmol Na(LNa), 5 or 12-13 mmol Na (CNa), 50 (HNa) or 120 mmol Na (vHNa) per 100 g food. Sodium appetite and water intake were about 50% higher in SHR than in WKY (4-4.5 vs 2.5-3 mmol Na per 100 g body wt day-1). It was modestly increased by both social stress and ACTH, and more so in WKY, thereby approaching that in SHR. Concerning the various Na diets and their influences, daytime resting MAP was modestly lowered in LNaSHR and slightly increased in vHNaSHR compared with CNaSHR but largely equal in all WKY groups. Food-water consumption was concentrated to the active night period, but even high Na-water intakes caused no signs of sustained hypervolaemia, because each intake bout was in both SHR and WKY eliminated by urine within 30-40 min. However, particularly the vHNa diet in SHR also increased the frequency of drinking, and each bout caused transient, evidently neurogenic MAP and HR increases which occurred too rapidly to be consequences of blood volume expansion. As a result, the diurnal MAP-HR patterns in SHR varied markedly with the Na diets, in vHNa group resulting in considerably raised average diurnal MAP levels even though resting daytime MAP was here nearly the same as in CNaSHR. These findings illustrate how largely continuous diurnal recordings are needed to judge correctly the relationships between, for example, Na intake, volume equilibrium and MAP. Finally, the relevance of these results in rats for also judging the control of Na balance in man is discussed.

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Handling of a Salt Load by Hypertensive and Normotensive Rats on Normal and Low Intakes of Sodium

Cited by 6 publications

References 0 publications

Vasopressin regulation of blood pressure and volume: findings from V1a receptor–deficient mice

Vasopressin regulation of blood pressure and volume: findings from V1a receptor–deficient mice

Vascular atrial natriuretic factor receptors in spontaneously hypertensive rats

Sodium appetite as well as 24‐h variations of fluid balance, mean arterial pressure and heart rate in spontaneously hypertensive (SHR) and normotensive (WKY) rats, when on various sodium diets

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