Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension.

Jeffries, William B.; McArdle, S; Bockman, Charles S.; Abel, Peter W.; Pettinger, William A.

doi:10.1161/01.hyp.17.1.63

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…Similar changes to renal structure have been reported by others. 21 The DOCA-salt-treated animals had elevated plasma sodium and osmolality levels, which is consistent with the observations that this model of hypertension is associated with increased renal sodium and water reabsorption 22 and with expansion of extracellular fluid volume. 23 The hypertensive animals also had elevated plasma AVP levels, a finding that has been reported previously by others 1 -2 and is probably due to an increased synthesis of AVP in the supraoptic and paraventricular nuclei of the hypothalamus.…”

Section: Resultssupporting

confidence: 87%

Regulation of vasopressin receptors in deoxycorticosterone acetate-salt hypertension.

et al. 1992

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Since arginine vasopressin may play a role in mlneralocorticoid hypertension, we examined the effects of deoxycorticosterone acetate (DOCA)-salt on vasopressin V, and V 2 receptor binding and their second messengers, inositol phosphate and adenylate cyclase, respectively, in liver and kidney to determine whether altered vasopressin receptor binding is pathogenetic in mineralocorticoid hypertension. The mean arterial blood pressure of mineralocorticoid (DOCA-salt)-treated rats (163±1 mm Hg) was increased compared with control salt-treated rats (salt) (122±1 mm Hg) and water-treated rats (120±l mm Hg;p<0.001). Mineralocorticoid treatment also increased plasma sodium, osmolality, and vasopressin concentration (p< 0.001). In the hypertensive animals, there was a reduction in hepatic V, (DOCA-salt, 91 ±12; salt, 132 ±13; and water, 145 ±13 fraol/mg protein; p<0.05) and renal V 2 receptor binding density (DOCA-salt, 53±5; salt, 93±9; and water, 95±9 fraol/mg protein; p<0.01), although receptor affinities remained unaltered. In contrast, the density of renal V, receptors was increased by mineralocorticoid treatment (DOCA-salt, 24±2; salt, 16±2; water, 18±1 fmol/mg protein; p<0.05), although the affinity was unchanged. Downregulation of V 2 receptors was associated with a decrease in maximum cyclic adenosine monophosphate levels (DOCA-salt, 19±4; salt, 49±6; water, 53±9 pmol • mg protein" 1 • 10 min~';p<0.05), whereas changes in V, receptor levels were not associated with changes in maximum inositol phosphate levels. Therefore, changes in plasma vasopressin levels rather than changes in vasopressin receptors and their maximum second messenger levels are more likely to play a role in the development of mineralocorticoid hypertension. 2 -4 Also the administration of an AVP antibody reduces blood pressure.1 -5 However, the strongest evidence is obtained from experiments using the Battleboro rat, which is unable to synthesize functional AVP and does not develop hypertension when treated with DOCA-salt. 56AVP mediates its physiological effects through two types of membrane-bound receptors that have been classified Vi and V 2 . The V! receptors are located in many tissues, including the vasculature, brain, liver, and kidney, are coupled to inositol phosphate turnover, and mediate the vasopressor and grycogenolytic effects of AVP. The V 2 receptors are found mainly in the kidney, are linked to adenylate cyclase and the production of cyclic adenosine monophosphate (cAMP), and are associated with antidiuresis.7 However, V 2 agonists also have extrarenal effects, including increased plasma factor VIII and von Willebrand factor levels 8 and vasodilatation. 9The importance of V] receptors in DOCA-salt hypertension is unclear. The reported effects of V, antagonists have been contradictory; studies suggest that these peptides produce moderate reductions 610 or no change 1112 in blood pressure in DOCA-salt-treated animals. However, V 2 receptors appear to be involved in the development of DOCA-salt hypertension since the use of a V 2 ...

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Section: Resultssupporting

confidence: 87%

Regulation of vasopressin receptors in deoxycorticosterone acetate-salt hypertension.

et al. 1992

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“…On the contrary, high-salt intake alone did not affect the cAMP generation in response to AVP. This finding is in agreement with that was observed by previous investigators, in which dietary salt intake in the absence of DOCA had no effect on the cAMP response to AVP (19). Taken together, basal as well as stimulated adenylate cyclase activity may be specifically augmented by DOCA.…”

Section: Reprintssupporting

confidence: 93%

“…However, it has been shown that DOCA-induced hypertension is dependent on excess dietary salt (19). Furthermore, a significant hypertension is lacking in syndrome of inappropriate antidiuretic hormone, although AQP2 expression is increased (22,23).…”

Section: Aquaporin-2 Water Channels In Hypertension 537mentioning

confidence: 99%

Increased Expression and Shuttling of Aquaporin-2 Water Channels in the Kidney in Doca-Salt Hypertensive Rats

Lee

Kang

Kim

2000

Clinical and Experimental Hypertension

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An altered role of AQP2 water channels in DOCA-salt hypertension was investigated. DOCA-salt hypertension was induced in rats. Control groups were either treated with DOCA alone or subjected to a high-salt intake without DOCA. Four weeks after inducing the hypertension, AQP2 expression and shuttling were determined in the kidney. Adenylate cyclase activity was also determined to examine the upstream affecting the AQP2 system. The AVP-evoked cAMP generation in the cortex and outer medulla was augmented following the treatment with DOCA either alone or combined with high-salt intake. Accordingly, the expression and shuttling of AQP2 proteins were increased in the cortex and outer medulla. These findings suggest that DOCA enhances cAMP generation and expression/shuttling of AQP2 water channels in the kidney, which may be causally related with the development of hypertension.

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“…Recently it has been shown that the enhanced vasopressin-stimulated accumulation of cyclic adenosine monophosphate in cortical collecting tubules seen in DOC-salt-treated Wistar rats is also present in DOCsalt-treated WF rats, despite their resistance to hypertension. 20 This study provides additional evidence that some physiological responses to mineralocorticoids are preserved in WF rats.…”

Section: Resultsmentioning

confidence: 57%

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

Bruner

1992

Hypertension

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Wistar-Furth rats have been shown to be resistant to mineralocortlcoid-salt hypertension, but the mechanism for this resistance is unknown. In the current experiments, adult male Wistar and Wistar-Furth rats were given a subcutaneous aldosterone infusion (0.15 /ig/hr) for 4 weeks, and changes in blood pressure and vascular reactivity were studied. Rats received a 1% NaCI, 0.2% KC1 solution to drink. After 4 weeks of aldosterone infusion, systolic blood pressure measured using a tail-cuff technique had increased by 60 mm Hg in Wistar rats but was unchanged in Wistar-Furth rats. Hypokalemia occurred in both strains in response to the aldosterone infusion. Isolated, helically cut strips of common carotid artery and aorta were prepared for isometric force recording. Cumulative concentration-response curves to norepinephrine, serotonin, KCI, calcium, nitroprusside, and acetylcholine were performed in carotid artery strips, and concentration-response curves to ouabain were performed in aortic strips. Increased vascular contractile sensitivity to KCI, ouabain, norepinephrine, and serotonin was observed in vessels from Wistar rats treated with aldosterone and salt The same treatment in Wistar-Furth rats produced only increased vascular sensitivity to ouabain and serotonin, and these changes were of smaller magnitude than those seen in Wistar rats. Aldosterone-salt treatment produced decreased vascular sensitivity to acetylcholine and nitroprusside in both Wistar and Wistar-Furth rats. These results support the hypothesis that resistance of Wistar-Furth rats to aldosterone-salt hypertension is due to resistance to the effects of aldosterone-salt treatment that normally result in increased vasoconstrictor sensitivity. espite long-standing recognition that hypertension can be produced by mineralocorticoid excess, the physiological mechanisms that contribute to the genesis and maintenance of such hypertension are still a matter of debate. One factor that has been suggested to contribute to mineralocorticoid-salt hypertension in experimental animals is changes in the sensitivity of vascular smooth muscle to vasoactive stimuli. An increase in sensitivity to vasoconstrictors such as norepinephrine and serotonin has been demonstrated in vascular preparations from mineralocorticoid-salt-treated rats, 1 " 4 and in some cases these vascular changes have been shown to precede the development of elevated blood pressure.5 - 6 The changes in vascular reactivity do not seem to be secondary to hypertension per se because protection of vascular beds from high pressure by proximal arterial ligation or antihypertensive therapy does not prevent the appearance of such changes. It recently has been reported that hypertension does not develop in response to the administration of excess deoxycorticosterone (DOC) and salt in the WistarFurth (WF) rat strain. 9 The current experiments were designed to test the hypothesis that a lack of development of changes in vascular reactivity is a mechanism involved in the resistance of WF rats to this form o...

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Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension.

Cited by 11 publications

References 24 publications

Regulation of vasopressin receptors in deoxycorticosterone acetate-salt hypertension.

Regulation of vasopressin receptors in deoxycorticosterone acetate-salt hypertension.

Increased Expression and Shuttling of Aquaporin-2 Water Channels in the Kidney in Doca-Salt Hypertensive Rats

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

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