Acid and alkaline phosphatase activities and calcium transport in aortic smooth muscle from DOCA hypertensive rats

Twietmeyer, T A; Bhalla, Ramesh C.; Maynard, Jerry A.

doi:10.1016/0022-2828(78)90357-7

Cited by 11 publications

(4 citation statements)

References 18 publications

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“…There has been much interest recently in the role of calcium in the pathogenesis of hypertension [10,11] and in the production of vascular lesions. In deoxycorticosterone (DOC)-induced hypertension, previous studies have shown an increase in the content of total calcium in the aorta [12,13] which is confirmed in the present study.…”

Section: Discussionsupporting

confidence: 90%

Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension

Yang

Nickerson

1988

Res. Exp. Med.

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Parathyroidectomy (Px) did not prevent the development of deoxycorticosterone (DOC)-induced hypertension inasmuch as the systolic blood pressure at 4 weeks did not differ from that of parathyroid intact, DOC-treated rats. Px, however, ameliorated the percent incidence and severity index of hypertension-induced vascular lesions in the heart and kidney. There was less hyaline change in the coronary artery and renal arteriole and fewer scars in the myocardium of Px + DOC rats than in DOC-treated animals. Arterial hypertrophy in aorta, coronary artery, renal interlobular artery, and renal arteriole in hypertensive animals was not affected by Px. The aortic content of total calcium in the Px-hypertensive rats was reduced significantly as compared to parathyroid-intact hypertensive rats. The abdominal aorta in the Px + DOC group showed a greater reduction in calcium than the thoracic aorta. We conclude that calcium may not be essential in mediating hypertension-induced vascular hypertrophy. Parathyroidectomy permitted a separation of high blood pressure-hypertrophy from hyaline vascular lesions in DOC-induced hypertensive rats, likely acting upon endothelial cells to prevent movement of plasma proteins (hyaline change) from the vascular lumen into the media-subendothelial space of blood vessels.

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Section: Discussionsupporting

confidence: 90%

Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension

Yang

Nickerson

1988

Res. Exp. Med.

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“…Measurements of total Ca2+ content in vessels from animals with DOCA/salt-induced hypertension and renovascular hypertension [26, 32, 77, cf. 59] as well as Ca2+ transport studies in DOCA/salt-induced hyper tension [40,41,54,78] revealed similar abnormalities to those seen in primary hypertension. These findings sup port the possibility that changes in intracellular free Ca2+ in smooth muscle may be the common last step in several forms of hypertension.…”

Section: Objections Against the 'Calcium Theory'mentioning

confidence: 58%

Calcium and Primary Hypertension

Zidek

Vetter²

1987

Nephron

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The role of dietary calcium in essential hypertension remains controversial. Various studies have found on the one hand a weak negative correlation between blood pressure and Ca²⁺ intake in special groups, and on the other hand a positive correlation between serum Ca²⁺ concentration and blood pressure. Several disturbances of cellular Ca²⁺ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca²⁺ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca²⁺ transport has been proposed as a mechanism. However, disturbances in cellular Ca²⁺ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca²⁺ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still unidentified humoral factor.

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“…However, en hanced 5'-nucleotidase, Mg2+-ATPase and alkaline phosphatase activities have been re ported to be associated with plasma mem brane-enriched fractions isolated from aorta [Wei et al, 1976;Twietmeyer et al, 1978Twietmeyer et al, , 1979 and mesenteric arteries [Kwan et al, 1979a[Kwan et al, , 1980a from hypertensive rats. It has been suggested that increased 5'-nucleotidase and alkaline phosphatase activities may contribute in part to the enhanced synthetic activities leading to thickening of blood ves sel walls as an adaptation to an increase in wall stress resulting from elevated blood pressure [Zemplenyi, 1968;Kwan et al, 1979a].…”

Section: Discussionmentioning

confidence: 99%

Abnormal Biochemistry of Subcellular Membranes Isolated from Nonvascular Smooth Muscles of Spontaneously Hypertensive Rats

Kwan¹,

Grover²,

Sakai³

1982

J Vasc Res

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Microsomal fractions enriched in plasma membranes and endoplasmic reticulum were isolated from stomach fundus and vas deferens from age-matched Okamoto spontaneously hypertensive (SHR) rats and corresponding Kyoto-Wistar normotensive rats (KWR). Alterations of several enzyme activities and Ca²⁺ accumulation of the isolated microsomal fraction from these nonvascular smooth muscles provide direct evidence of abnormal smooth muscle membrane biochemistry in SHR. Decreased Ca²⁺ accumulation in the presence of but not in the absence of adenosine triphosphate by the microsomal fractions of both fundus and vas deferens from SHR is consistent with previous findings using plasma membranes from vascular smooth muscles from SHR and cannot be explained in terms of adaptation induced by elevation of blood pressure in SHR. Defective Ca²⁺ handling now observed in both vascular and nonvascular smooth muscles from hypertensive animals not only provides a cellular basis for the altered reactivity and contractility of smooth muscles observed in SHR, but also supports the hypothesis that spontaneous hypertension is associated with a generalized widespread alteration in smooth muscle membrane fraction.

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Acid and alkaline phosphatase activities and calcium transport in aortic smooth muscle from DOCA hypertensive rats

Cited by 11 publications

References 18 publications

Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension

Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension

Calcium and Primary Hypertension

Abnormal Biochemistry of Subcellular Membranes Isolated from Nonvascular Smooth Muscles of Spontaneously Hypertensive Rats

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