Mechanism of acute hypercalcemic hypertension in the conscious rat.

Berl, Tomás; Levi, Moshe; Ellis, M. A.; Chaimovitz, Cidio

doi:10.1161/01.hyp.7.6.923

Cited by 22 publications

(17 citation statements)

References 38 publications

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“…Previous studies in our lab oratory have shown that acute hypercalcemia causes a dose-related rise in blood pressure. However, we also showed that increases in serum calcium in the order of magnitude used in the present study were not associated with any significant change in blood pressure [3], In addi tion. evidence is available in animals and in man that subpressor doses of calcium cause no changes in cardiac out put or in systemic vascular resistance, whereas pressor 90 Liu/Bigazzi/Ballard/Campese Hypercalcemia and RSNA * p < 0.05 (Anova) compared to rats given calcium or a-methyltyrosine.…”

Section: Discussionsupporting

confidence: 50%

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

et al. 1992

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Since calcium plays a modulatory role in the activity of the sympathetic nervous system (SNS), in these studies, we have tested the hypothesis that hypercalcemia may alter renal SNS activity, and, consequently, renal function. Acute hypercalcemia was induced in Sprague-Dawley rats by infusion of calcium 30mg/kg/2h in 0.45% saline. A control group of rats received only 0.45 % saline. Two more groups of rats received either calcium or 0.45 % saline 7-10 days after total renal denervation. Calcium infusion increased serum calcium by 1.8 ± 0.23 mg/dl in rats with intact renal nerves and by 2.7 ± 0.48 mg/dl in renal denervated rats. Mean arterial pressure and inulin clearance did not change during calcium or 0.45% saline in rats with intact renal nerves. Renal sympathetic nerve activity (RSNA) decreased by 44% in rats infused with calcium, but it did not change in control animals. Calcium caused a significantly greater rise in urine volume, sodium excretion and fractional excretion of sodium than the infusion of 0.45% saline. Rats with renal denervation manifested greater baseline urine volume, sodium excretion and fractional excretion of sodium than rats with intact renal nerves. Infusion of calcium, however, caused no further rise in urine sodium excretion in these animals. α-Methyltyrosine, an inhibitor of norepinephrine (NE) synthesis, also increased natriuresis in rats. Calcium reduced by 27% the NE content in the kidney but not in the heart. Methyltyrosine, on the other hand, reduced NE content in both the heart and the kidney. These data demonstrate that acute hypercalcemia inhibits RSNA and increases diuresis and natriuresis in the absence of any change in blood pressure or in glomerular filtration rate.

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Section: Discussionsupporting

confidence: 50%

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

et al. 1992

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“…34 In another study, 30 the mean blood pressure increment in Wistar rats given a much larger calcium load was only +12 mm Hg (112±3->124±5 mm Hg) despite a serum calcium that was twice that of the Sprague-Dawley rats (24.9±1.2 mg/dl). This suggests that the pressor responsiveness to hypercalcemia is blunted in Wistar rats.…”

Section: Figure 2 Bar Graph Of Plasma Atrial Natriuretic Factor (Anpmentioning

confidence: 94%

Calcium infusion increases plasma atrial natriuretic factor in spontaneously hypertensive rats.

1989

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The effect of calcium on plasma atrial natriuretic factor (ANF) concentration was determined in spontaneously hypertensive rats (SHR) and their control, Wistar-Kyoto (WKY) rats. CaCl 2 10.5 mg (0.095 mmol) in 0.54 ml 5% glucose or an equal volume of vehicle alone was infused intravenously for 30 minutes into conscious precannulated SHR (vehicle, n=16; CaCl 2 , n=16) and WKY rats (vehicle, n=25; CaCl 2 , n=15). Direct systolic blood pressure was measured throughout the infusion period. Blood samples for serum total calcium and plasma ANF were obtained at the end of each experiment. The systolic blood pressure did not change significantly during infusion of the vehicle or CaCl 2 in either strain. No significant difference was observed in serum total calcium concentration between SHR and WKY rats after vehicle (9.8 ±0.1 [mean±SEM] mg/dl vs. 10.0±0.1) or after CaCl 2 infusion (12.2±0~3 vs. 12.2±0.2). Plasma ANF concentrations after both vehicle and CaCl 2 infusion were significantly higher in SHR than in WKY rats (vehicle, 211±24 pg/ml vs. 129±ll,p<0.05; CaCl 2 ,395±21 vs. 278±33,p<0.05). There were high degrees of correlation between serum total calcium and plasma ANF both in SHR (r=0.77, /><0.001) and in WKY rats (r=0.76, p<0.001). No significant difference was observed in the slopes of the regression lines of ANF as a function of the serum total calcium concentration between SHR and WKY rats. Additionally, no significant correlation was observed between blood pressure at 30 minutes and plasma ANF levels in SHR or in WKY rats. These data indicate that acute hypercalcemia in the absence of significant changes in blood pressure is a potent stimulus for ANF release in the rat. Despite higher basal ANF levels, the SHR maintain a response similar to that in WKY rats. (Hypertension 1989;14:98-103)

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“…17 Acutely induced hypercalcemia in conscious rats causes hypertension and is reported to be without any involvement of catecholamines. 33 Other reports, however, indicate that catecholamines are involved in hypertension induced by hypercalcemia. 13 ' l6 -M Our laboratory has reported that dietary calcium deficiency does not alter the noradrenergic response of atria in rats, 33 but vitamin D deficiency does.…”

Section: Figure 2 Depressor Response To Parathyroid Hormone (Pth-[1 mentioning

confidence: 99%

“…33 Other reports, however, indicate that catecholamines are involved in hypertension induced by hypercalcemia. 13 ' l6 -M Our laboratory has reported that dietary calcium deficiency does not alter the noradrenergic response of atria in rats, 33 but vitamin D deficiency does. We believe that when more studies are done a clear picture of catecholamine involvement will emerge.…”

Section: Figure 2 Depressor Response To Parathyroid Hormone (Pth-[1 mentioning

confidence: 99%

“…31 On the other hand, Zawada et al 32 reported that TPTX in dogs reduced MAP as well as plasma calcium. Hypercalcemia of acute 33 or chronic duration 31 has a different effect on BP. The high Ca (2.8%) diet group, which had a reduced hypotensive response, also snowed higher plasma calcium levels and nondetectable PTH levels compared with the TPTX group, which showed both reduced plasma calcium and nondetectable PTH (see Figure 2).…”

Section: Figure 2 Depressor Response To Parathyroid Hormone (Pth-[1 mentioning

confidence: 99%

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Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

Baksi

1988

Hypertension

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SUMMARY Experimental and clinical data suggest an association between chronic hyperparathyroidism and hypertension, but acute infusion of parathyroid hormone causes vasodilation and hypotension. These observations imply that chronic and acute parathyroid states affect blood pressure through different mechanism(s), either by modification of vascular receptors or by an ionophoretic effect of parathyroid hormone. The effect of parathyroid status induced by dietary calcium manipulations or by surgical ablation of the parathyroid gland on the hypotensive response of parathyroid hormone infusion was studied in rats. At 4 weeks of age 24 male rats were divided into four equal groups. Three groups were sham-operated, and one group was thyroparathyroidectomized. Only the thyroparathyroidectomized group was treated with thyroxine, 10 /xg/kg/day. The control and thyroparathyroidectomized groups were raised on a 1.4% calcium diet; the other two groups were raised on 0.005% and 2.8% calcium diets. After 8 weeks on the diets, parathyroid hormone was infused through a venous cannula at 5 and 10 ng/kg doses and blood pressure was measured through arterial cannulas. The results indicate that hyperparathyroidism and hypocalcemia induced by the low calcium diet attenuated the hypotensive response to parathyroid hormone compared with responses in rats raised on a 1.4% calcium diet. In hypoparathyroid rats (2.8% Ca diet) with hypercalcemia, the hypotensive response was also reduced. However, in hypoparathyroid (thyroparathyroidectomized) rats with hypocalcemia, the hypotensive response was enhanced. The data suggest that chronic parathyroid status, as well as hypercalcemia, alters the hypotensive response to parathyroid hormone infusion, presumably by altering the vascular parathyroid hormone receptors or by some other mechanism. (Hypertension 11: 509-513, 1988 Yet hyperparathyroidism is often associated with increased BP in humans 6 " 8 and rats. 9 "" The cellular basis for chronic PTH action on BP regulation is unknown.12 " 14 PTH may influence the sympathetic nervous system and vasoactive hormones either directly or indirectly through changes in plasma ionic cal- cium. 15 ' l6 The accentuation of hypertension by hyperparathyroidism or long-term PTH administration, blunted vascular reactivity in the hypercalcemic state, 17 and hypocalcemia after parathyroidectomy are all consistent with the hypothesis that PTH exerts an ionophoretic and, therefore, a permissive effect on the vasoconstrictive and hypertensive action of extracellular fluid calcium.18 " 20 The purpose of the present study was to investigate the effect of long-term modifications of PTH status by surgical and dietary means in normotensive Sprague-Dawley rats on the hypotensive response to acute PTH administration. In addition, the plasma and bone calcemic parameters were measured to document the alterations in systemic calcium metabolism and PTH status.

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Mechanism of acute hypercalcemic hypertension in the conscious rat.

Cited by 22 publications

References 38 publications

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

Calcium infusion increases plasma atrial natriuretic factor in spontaneously hypertensive rats.

Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.

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