Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

Berthelot, Alain; Gairard, A.

doi:10.1042/cs0580365

Cited by 40 publications

(11 citation statements)

References 10 publications

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“…We have thus confirmed previous results from this laboratory (Berthelot & Gairard, 1980). Reid, Zivin & Kopin (1975) and De Champlain, Farley, Cousineau & Van Ameringen (1976) found increased concentrations of serum catecholamines in DOCA-andsaline-induced hypertension.…”

Section: Discussionsupporting

confidence: 81%

Relation Between Calcium and Cardiovascular Reactivity in Mineralocorticoid‐induced Hypertension in the Rat

Berthelot¹,

Gairard²,

Goyault³

et al. 1980

British J Pharmacology

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1 Previous work has shown that parathyroidectomy (PTX) decreases cardiovascular reactivity to noradrenaline in Sprague-Dawley rats with mineralocorticoid-induced (D) hypertension. 2 In order to explain this diminution of cardiovascular reactivity, we studied in vivo the influence of serum calcium levels on the cardiac and vascular response to noradrenaline (500 ng/kg). We used rats with or without parathyroids but fed a standard or a high-calcium (+Ca) diet that re-established a serum calcium level of about 100 mg/l. Work was performed in vagotomized, anaesthetized rats after ganglionic blockade with pentolinium and atropine sulphate. 3 Cardiac output was unchanged in all the experimental groups after 11 weeks of mineralocorticoid treatment. The enhancing effect of noradrenaline was not modified. 4 Since a serum calcium level of about 100 mg/l was sufficient to re-establish vascular reactivity to exogenous noradrenaline in the PTX-D rats, parathyroid hormone was not necessary. 5 The total and lanthanum-resistant calcium fractions of the walls of the aorta were reduced in the PTX-D rats. When serum calcium levels were re-established at about 100 mg/l, there was no difference between PTX-D and D rats. 6 It is postulated that the decreased storage of calcium in vascular smooth muscle cells of PTX-D rats depresses the vascular effect of noradren4line.

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Section: Discussionsupporting

confidence: 81%

Relation Between Calcium and Cardiovascular Reactivity in Mineralocorticoid‐induced Hypertension in the Rat

Berthelot¹,

Gairard²,

Goyault³

et al. 1980

British J Pharmacology

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“…Studies of the spontaneously hypertensive rat (SHR) model of hypertension suggest that PTH is a factor in the development of hypertension. 32 ' 33 In this regard, parathyroidectomy can ameliorate the degree of blood pressure rise in SHR. 34 Other studies in the rat have indicated that PTH exerts a permissive role in the pressor effect of calcium infusion.…”

Section: Discussionmentioning

confidence: 99%

Calcitropic hormones, platelet calcium, and blood pressure in essential hypertension.

et al. 1990

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Plasma ionized calcium, platelet cytosolic calcium (using the fura-2 method in gel-filtered platelets), parathyroid hormone (both the intact hormone and a midmolecule portion), calcitriol, and calcidiol were measured in 19 untreated male patients with essential hypertension and 19 age-matched normotensive male research subjects. Mean levels of platelet cytosolic calcium, parathyroid hormone, calcitriol, and calcidiol were all significantly higher, whereas plasma ionized calcium was significantly lower, in the hypertensive group compared with the normotensive group. Both platelet cytosolic calcium and intact parathryoid hormone were positively correlated with mean arterial pressure (r=0.58, /?<0.001; r=0.S4, p<0.001, respectively), whereas plasma ionized calcium was inversely correlated with mean arterial pressure (r=-0.60, p<0.001) in the combined group of all study subjects. All three of these correlations were significant in the hypertensive group alone but not in the normotensive group alone. When analyzed with plasma ionized calcium, body mass index, serum calcitriol, and calcidiol in a multivariable regression model, the significance of the partial regressions of platelet cytosolic calcium and parathyroid hormone with mean arterial pressure persisted. Intact parathryoid hormone was positively correlated to platelet cytosolic calcium (r=0.43, p<0.01) and plasma ionized calcium was inversely correlated to platelet cytosolic calcium (r= -0.44,p<0.01). These results confirm previous reports of disturbances of calcium metabolism in essential hypertension and suggest that the elevated platelet cytosolic calcium observed in essential hypertension may be linked to one or more of these alterations of calcium metabolism. {Hypertension 1990;16:515-522) S everal studies have described disturbances of calcium metabolism in subjects with essential hypertension. McCarron 1 reported decreased plasma ionized calcium in patients with essential hypertension and also suggested that subjects with essential hypertension include less calcium in their diet.2 Further, McCarron and Morris 3 also found that supplementing the dietary calcium intake of subjects with essential hypertension could decrease the blood pressure of some subjects. The blood pressure-lowering effect of dietary calcium has also been observed in rat models of hypertension.

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“…While a hypotensive effect of acute intravenous administration of PTH has been demonstrated in by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from both rats and dogs, chronic ablation of the parathyroid glands has been shown to attenuate experimental mineralocorticoid-induced hypertension. 48 In a recently reported study with SHR, we demonstrated that parathyroidectomy was associated with a significant attenuation in the rise in blood pressure in SHR, but had no effect on that of the WKY rat. 21 In summary, we have provided evidence of hyperparathyroidism in the SHR, having observed parathyroid hyperplasia and histological evidence of its effect on bone.…”

Section: Quantitative Bone Histologymentioning

confidence: 99%

Hyperparathyroidism and abnormal calcitriol metabolism in the spontaneously hypertensive rat.

et al. 1989

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Received February 12, 1988; accepted October 31, 1988. Kyoto (WKY) rat. '-6 The involvement of the two principal hormones regulating calcium metabolism, parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D 3 (calcitriol), in these abnormalities remains uncertain. Several groups, including ourselves, have provided evidence of abnormal calcitriol metabolism in the SHR, 7 -12 but measurements of tissue calcitriol receptors have not been provided.The relation between abnormal calcitriol metabolism and hypertension in the SHR remains uncertain, but recent evidence suggests that this relation is more than indirect. The existence of specific calcitriol receptors in preparations derived from vascular smooth muscle has been demonstrated by our group 1314 and others. 13 These observations raise the possibility that calcitriol may play a role in regulating vascular smooth muscle function analogous to its role in skeletal muscle, where specific calcitriol receptors have also been identified. 16 In this context, the recent demonstration of raised by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from

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Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

Cited by 40 publications

References 10 publications

Relation Between Calcium and Cardiovascular Reactivity in Mineralocorticoid‐induced Hypertension in the Rat

Relation Between Calcium and Cardiovascular Reactivity in Mineralocorticoid‐induced Hypertension in the Rat

Calcitropic hormones, platelet calcium, and blood pressure in essential hypertension.

Hyperparathyroidism and abnormal calcitriol metabolism in the spontaneously hypertensive rat.

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