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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both calcium and parathyroid hormone appear to be involved in the acute and chronic regulation of arterial pressure in experimental animals and humans. While the direct evidence is still preliminary, the net effect of calcium and parathyroid hormone under normal physiologic conditions is to favor a reduction in blood pressure. The implications of this assessment for common medical disorders, such as essential hypertension, and less common but oftentimes more challenging clinical conditions, such as end-stage renal disease, are potentially substantial.
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PMID:Calcium, parathyroid hormone, and hypertension. 257 35

Patients with essential hypertension, in particular those with low plasma renin activity (PRA), are reported to have lowered plasma-ionized calcium and elevated parathyroid hormone levels. In this study 1 microgram alphacalcidol (1 alpha-hydroxy-vitamin D3) was given in a double-blind, placebo-controlled fashion over four months to 39 subjects with mild to moderate hypertension. There was a significant rise in PRA in the treatment group when compared to placebo (P less than .05), but the mean blood pressure response was similar in the two groups. When the treatment group was divided according to pretreatment PRA it was, however, seen that subjects with low PRA displayed a reduction in diastolic blood pressure, whereas those with high PRA raised their blood pressure compared to placebo. Also subjects with low pretreatment values for plasma-ionized calcium and high levels of parathyroid hormone showed a reduction in diastolic blood pressure. This study supports the idea of a relationship between calcium metabolism and the renin-aldosterone system in essential hypertension and describes a beneficial effect of vitamin D supplementation on blood pressure in low-renin hypertension.
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PMID:Reduction of blood pressure during long-term treatment with active vitamin D (alphacalcidol) is dependent on plasma renin activity and calcium status. A double-blind, placebo-controlled study. 264 69

The relationship between changes in the pressor response to infused noradrenaline induced by intravenous injection of ouabain, an Na+,K+-ATPase inhibitor, and plasma renin activity and plasma ionized calcium was examined in 16 normotensive subjects and in 16 patients with essential hypertension. These patients were divided into 11 normal-renin and five low-renin essential hypertensives. The pressor response was significantly greater in low-renin hypertensives than in normotensives and normal-renin hypertensives. Following the injection of ouabain, the pressor response was significantly increased with no change in basal levels of blood pressure, plasma noradrenaline concentration, plasma calcium and plasma parathyroid hormone in both normotensives and essential hypertensives. The pressor response to noradrenaline was negatively correlated with levels of plasma noradrenaline and calcium after the injection of ouabain as well as before the injection in normotensives and essential hypertensives. The regression line between the pressor response and that of plasma noradrenaline or plasma calcium was significantly shifted towards a higher pressor response in normotensives, but not in essential hypertensives. The changes in the pressor response to noradrenaline induced by the injection of ouabain was significantly smaller in essential hypertensives, particularly in low-renin hypertensives, compared with normotensives. These results suggest that: (1) ouabain increases the pressor response to noradrenaline; (2) this increase is related to calcium metabolism; (3) endogenous Na+,K+-ATPase inhibitor(s) might be elevated in essential hypertensives; and (4) an increase in endogenous Na+,K+-ATPase inhibitor might, therefore contribute to an enhanced noradrenaline response in essential hypertensives, particularly in low-renin hypertensives.
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PMID:The effect of ouabain on pressor responses to infused noradrenaline in patients with essential hypertension. 285 44

A role for calcium in human hypertensive disease has been suggested. However, the various, apparently contradictory, abnormalities of calcium metabolism observed in experimental and clinical hypertension do not allow for unambiguous description of the specific manner in which calcium contributes to the hypertensive process. We studied calcium metabolism in essential hypertension and used renin-sodium profiling, which reveals the biochemical heterogeneity of clinical hypertension. We observed renin-linked, heterogeneous deviations in circulating levels of the divalent cations, magnesium and ionized calcium, in addition to deviations in the calcium-regulating hormones, parathyroid hormone (PTH), calcitonin (CT), and 1,25 dihydroxyvitamin D (1,25 D). These renin-calcium metabolic deviations may both predict and contribute to the pathophysiology of salt-induced hypertension, the blood pressure effects of oral calcium supplementation, as well as the short and longer term effectiveness of calcium channel blockade. Altogether, these data suggest an intimate linkage between the hormonal control of calcium metabolism, the renin-angiotensin system and blood pressure regulation in human hypertension.
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PMID:The significance of calcium and calcium channel blockade in essential hypertension. 285 82

The renin-angiotensin-aldosterone system regulates blood pressure and volume homeostasis in addition to sodium and potassium metabolism, and may be linked to divalent cation metabolism as well as hypertensive disease. In essential hypertension, circulating serum magnesium and Ca++, and the calcium regulating hormones, parathyroid hormone, calcitonin and 1,25 dihydroxyvitamin (1,25D) are different in the various renin subgroups. Elevated blood pressure induced by such maneuvers as dietary salt loading is associated with exacerbations of these calcium metabolic deviations, and appears related to salt-induced changes in serum Ca++ or 1,25D levels. Short- or longer-term lowering of blood pressure with the calcium-channel blocker, nifedipine, or with calcium or magnesium supplementation is associated with a shift of renin system activity and calcium metabolic indexes back to average normotensive values in those subjects most susceptible to these hypotensive agents. These observations suggest that deviations in calcium metabolism in essential hypertension may be related to the pathophysiology of the hypertensive process. Further, renin system activity and calcium metabolic indexes such as serum Ca++ levels may help target specific subgroups of hypertensive populations most susceptible to various dietary or drug maneuvers, and thus may provide a basis to better understand and treat clinical hypertension.
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PMID:Renin, calcium metabolism and the pathophysiologic basis of antihypertensive therapy. 286 7

We have found increased renal alpha 2-adrenoceptor density and a defect in prostaglandin and parathyroid stimulated adenylate cyclase in two genetic forms of rat hypertension. Changes in serum calcium and parathyroid hormone (PTH) levels suggest biologic significance to this defective adenylate cyclase response. Our hypothesis is that one or more of these defects contribute to excess renal retention of sodium and increase vascular resistance of genetically hypertensive rats and humans with essential hypertension who have similar abnormalities of calcium and PTH.
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PMID:The role of renal catecholamines in hypertension. 298 54

Abnormal calcium (Ca) homeostasis has been reported in essential hypertension and in the Okamoto-Aoki strain of spontaneously hypertensive rats. These abnormalities include increased urinary excretion of calcium and decreased ionized serum calcium (Ca2+). To pursue these abnormalities we studied the chronology of urinary excretion of electrolytes in a genetically homogeneous strain of hypertensive rat, the Dahl/Rapp salt sensitive (S) and resistant (R) rat (at ages 3, 5, 7, 9, 12, 20 and 32 weeks). We also characterized the renal adenylate cyclase-cAMP system by measuring urinary cAMP excretion and adenylate cyclase response to membrane receptor agonists in renal membranes from S and R rats at day 2 and at 6 and 28 weeks of age. Urinary calcium excretion was higher in S than in R at 3, 5 and 7 weeks (0.48 +/- 0.04 versus 0.24 +/- 0.01 mg/mg creatinine at 7 weeks, P less than 0.01). Sodium and phosphorous excretion were lower in S than in R rats at 5, 7, 9, and 12 weeks, and at 5, 7, 9, 12, 20 and 32 weeks, respectively. Potassium excretion was similar in the two groups. Plasma ionized calcium was lower in S than in R rats (3.9 +/- 0.1 versus 4.5 +/- 0.1 mg/dl, P less than 0.01) only at 7 weeks of age. Plasma parathyroid hormone (PTH) was not different between S and R rats. Cyclic AMP excretion and the renal adenylate cyclase response to PTH when referenced to basal activity was lower in S than in R rats at all ages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered calcium homeostasis in Dahl hypertensive rats: physiological and biochemical studies. 300 3

Disorders of calcium and parathyroid hormone homeostasis have been reported in subjects with essential hypertension. In many of these studies, dietary intakes of sodium and calcium were not carefully controlled. The present study was designed to compare calcium and parathyroid hormone homeostasis in normal and hypertensive subjects on controlled dietary sodium and calcium intakes and to examine the impact of dietary sodium loading on hemodynamic and metabolic responses to infused calcium. Seven subjects with essential hypertension and seven age-matched and sex-matched controls were studied while consuming a standard diet containing 600 mg of elemental calcium. Each subject was studied while consuming 10, 160, and 510 mEq of sodium per day, before, during, and after a 3-hour calcium infusion (3.75 mg/kg/hr). Before calcium infusion, hypertensive subjects had increased urinary cyclic adenosine 3',5'-monophosphate excretion independent of sodium intake (p less than 0.05). Urinary potassium excretion was greater in normotensive than in hypertensive subjects (p = 0.002). At baseline, dietary sodium intake had no effect on systolic, diastolic, or mean arterial pressure. During calcium infusion, systolic pressure increased in both groups, whereas diastolic pressure increased only when dietary sodium content was high and mean arterial pressure increased only in hypertensive subjects (p = 0.007). Together, these data provide evidence for interactions between dietary sodium intake and the cardiovascular response to calcium. They confirm that hypertensive subjects exhibit enhanced parathyroid gland function even when dietary factors are controlled, and they suggest that these subjects are more sensitive to the cardiovascular effects of short-term calcium infusion.
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PMID:Effects of calcium infusion on blood pressure in hypertensive and normotensive humans. 301 65

In a double-blind, randomized, placebo-controlled, crossover trial, 23 middle-aged patients with mild to moderate essential hypertension were given an oral calcium supplement (1 g/day) for 8 weeks. At the end of this period, eight patients continued with this treatment for an additional 2 weeks but were also given 0.5 micrograms/day of 1,25-(OH)2 vitamin D3. In the 21 patients who completed the study, arterial pressure during the calcium-supplemented phase was almost identical to that of the placebo phase. In eight patients, mean arterial pressure (MAP) had changed by greater than 5 mmHg at the end of the calcium-supplemented period, compared with the end of the placebo phase (six patients showed an increase in MAP and two a decrease). Changes in arterial pressure were unrelated to age, plasma ionized calcium, parathyroid hormone (PTH), plasma renin activity (PRA), plasma aldosterone, 24-h urinary calcium, sodium and potassium and were only weakly related to body weight. In the eight patients who continued with the treatment of calcium plus 1,25-(OH)2 vitamin D3 after the 8-week study period, arterial pressure changed very little and not significantly. These results do not support the suggestion that calcium supplements lower arterial pressure in middle-aged subjects with mild to moderate essential hypertension.
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PMID:Double-blind randomized, crossover trial of calcium supplementation in essential hypertension. 304 2

The cause of hypertension in primary hyperparathyroidism and its response to corrective surgery remains a matter of controversy. We therefore studied blood pressure, vasoactive hormones and plasma calcium responses to parathyroidectomy in six hypertensive and two normotensive patients with primary hyperparathyroidism. Twenty-four-hour intra-arterial pressure recordings, together with hourly blood sampling for plasma renin activity (PRA), aldosterone, cortisol, catecholamines and calcium levels, were undertaken in each patient before surgery and were repeated under identical conditions 3-6 months after parathyroidectomy. Mean plasma calcium was 3.03 +/- 0.1 before, and 2.35 +/- 0.02 mmol/l after, parathyroidectomy. Changes in arterial pressure were small and variable in individual patients. Group mean arterial pressures before and after surgery were identical. Plasma cortisol and PRA were significantly higher in the hypercalcaemic state (P less than 0.01 and P less than 0.05, respectively) but there was no significant difference in plasma aldosterone or catecholamine levels. No correlations between changes in plasma calcium or parathyroid hormone levels and concomitant changes in plasma concentration of other hormones were observed. Our findings show that correction of primary hyperparathyroidism has no systematic effect on arterial pressure in a heterogeneous group, including some patients with probable background essential hypertension, when evaluated 3-6 months after surgery. Compared with values after corrective surgery, mean levels of PRA and cortisol-but not aldosterone or catecholamines--are elevated in patients with primary hyperparathyroidism. These findings are consistent with an inhibitory effect of raised ionic calcium concentration on the response of the adrenal glomerulosa to angiotensin and adrenocorticotrophic hormone.
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PMID:Hormone, calcium and blood pressure relationships in primary hyperparathyroidism. 305 96


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