High calcium diet augments vascular potassium relaxation in hypertensive rats.

Pörsti, Ilkka; Arvola, Pertti; Wuorela, Heikki; Vapaatalo, Heikki

doi:10.1161/01.hyp.19.1.85

Cited by 28 publications

(11 citation statements)

References 32 publications

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“…Just as Furspan and Bohr 210 observed lower levels of intracellular free calcium in lymphocytes from animals on high calcium diets, Porsti et al 183 reported lower levels of intracellular free calcium in platelets isolated from animals maintained on supplemental calcium diets. These favorable changes in intracellular calcium regulation may be related to increased Ca 2+ -ATPase activity.…”

Section: + -Atpasementioning

confidence: 95%

“…In a previous report, they noted that potassium-induced relaxation of mesenteric arterial rings was augmented by calcium supplementation in SHR. 183 Because ouabain was able to prevent the relaxation, the difference between diet groups was attributed to increased Na,K-ATPase activity. This outcome is consistent with the notion of a reciprocal relation between intracellular calcium and Na,KATPase activity; as intracellular calcium declines, Na,K-ATPase activity increases.…”

Section: Nak-atpasementioning

confidence: 99%

“…• References 116,128,129,141,177,183,184. enteric arterial rings was enhanced in calciumsupplemented animals, perhaps as a consequence of an increased ability to extrude calcium from the cell.…”

Section: + -Atpasementioning

confidence: 99%

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Dietary calcium and blood pressure in experimental models of hypertension. A review.

1994

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More than 80 studies have reported lowered blood pressure after dietary calcium enrichment in experimental models of hypertension. The evidence presented here suggests that dietary calcium may act concurrently through a number of physiological mechanisms to influence blood pressure. The importance of any given mechanism may vary depending on the experimental model under consideration. Supplemental dietary calcium is associated with reduced membrane permeability, increased Ca(2+)-ATPase and Na,K-ATPase, and reduced intracellular calcium. These results suggest that supplemental calcium may limit calcium influx into the cell and improve the ability of the VSMC to extrude calcium. This could be a direct effect of calcium on the VSMC or an indirect effect mediated hormonally. The calcium-regulating hormones have all been found to have vasoactive properties and therefore may influence blood pressure. Furthermore, CGRP and the proposed parathyroid hypertensive factor are both vasoactive substances that are responsive to dietary calcium. Therefore, diet-induced variations in calcium-regulating hormones may influence blood pressure. Modulation of the sympathetic nervous system is another important way that dietary calcium can influence blood pressure. There is evidence of altered norepinephrine levels in the hypothalamus as a consequence of manipulations of dietary calcium as well as changes in central sympathetic nervous system outflow. Dietary calcium has also been shown to specifically modify alpha 1-adrenergic receptor activity in the periphery. In some experimental models of hypertension, dietary calcium may alter blood pressure by changing the metabolism of other electrolytes. For example, the ability of calcium to prevent sodium chloride-induced elevations in blood pressure may be attributed to natriuresis. However, natriuresis does not account for all of the interactive effects of calcium and sodium chloride on blood pressure. Sodium chloride-induced hypertension may be due in part to calcium wasting and subsequent elevation of calcium-regulating hormones. Chloride is an important mediator of this effect because it appears that sodium does not cause calcium wasting when it is not combined with chloride. More attention to the central nervous system effects of dietary calcium is needed. Not only can calcium itself influence neural function, but many of the calcium-regulating hormones appear to affect the central nervous system. The influence of calcium and calcium-regulating hormones on central nervous system activity may have important implications for blood pressure regulation and also may extend to other aspects of physiology and behavior.

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Section: + -Atpasementioning

confidence: 95%

Section: Nak-atpasementioning

confidence: 99%

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Dietary calcium and blood pressure in experimental models of hypertension. A review.

1994

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“…Milk is rich in minerals (Ca, K), which most probably also contribute to the antihypertensive effect. For example, the antihypertensive effect of Ca has been shown quite uniformly in SHR (25,56,57) . Active milk significantly improved the endotheliumdependent relaxation of mesenteric arteries.…”

Section: Discussionmentioning

confidence: 99%

High blood pressure-lowering and vasoprotective effects of milk products in experimental hypertension

et al. 2011

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Milk casein-derived angiotensin-converting enzyme (ACE)-inhibitory tripeptides isoleucine-proline-proline (Ile-Pro-Pro) and valineproline-proline (Val-Pro-Pro) have been shown to have antihypertensive effects in human subjects and to attenuate the development of hypertension in experimental models. The aim of the present study was to investigate the effect of a fermented milk product containing Ile-Pro-Pro and Val-Pro-Pro and plant sterols on already established hypertension, endothelial dysfunction and aortic gene expression. Male spontaneously hypertensive rats (SHR) with baseline systolic blood pressure (SBP) of 195 mmHg were given either active milk (tripeptides and plant sterols), milk or water ad libitum for 6 weeks. SBP was measured weekly by the tail-cuff method. The endothelial function of mesenteric arteries was investigated at the end of the study. Aortas were collected for DNA microarray study (Affymetrix Rat Gene 1.0 ST Array). The main finding was that active milk decreased SBP by 16 mmHg compared with water (178 (SEM 3) v. 195 (SEM 3) mmHg; P,0·001). Milk also had an antihypertensive effect. Active milk improved mesenteric artery endothelial dysfunction by NOdependent and endothelium-derived hyperpolarising factor-dependent mechanisms. Treatment with active milk caused mild changes in aortic gene expression; twenty-seven genes were up-regulated and eighty-two down-regulated. Using the criteria for fold change (fc) , 0·833 or . 1·2 and P,0·05, the most affected (down-regulated) signalling pathways were hedgehog, chemokine and leucocyte transendothelial migration pathways. ACE expression was also slightly decreased (fc 0·86; P¼ 0·047). In conclusion, long-term treatment with fermented milk enriched with tripeptides and plant sterols decreases SBP, improves endothelial dysfunction and affects signalling pathways related to inflammatory responses in SHR.Key words: Milk-derived bioactive peptides: Experimental hypertension: Spontaneously hypertensive rats: Plant sterols: Endothelial function Hypertension is one of the most important risk factors for CHD, heart failure, cerebrovascular disease and chronic kidney disease. The prevalence of hypertension is increasing worldwide, both in developed and developing countries (1) . Up to 30 % of the world's adult population was estimated to have hypertension in 2000 (2) . Any reductions in blood pressure, however small, are meaningful; a systolic blood pressure (SBP) reduction of 9 mmHg and a diastolic blood pressure reduction of 5 mmHg reduce the risk of stroke by [35][36][37][38][39][40] .Besides pharmacological therapy, lifestyle and nutritional factors play a significant role in the prevention and treatment of hypertension and related disorders. Low saturated fat and Na intake and increased consumption of K, Ca and soluble fibre positively affect blood pressure (4) . Plant sterols and stanols (also called as phytosterols and -stanols) have wellestablished cholesterol-lowering effects. The consumption of 2 g plant sterols per d has been shown to lowe...

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“…Thereafter atenolol administration was withdrawn 1 day before the rats were decapitated and exsanguinated. The blood samples were drawn into polystyrene tubes containing heparin (100units ml-') as anticoagulant for lymphocyte intracellular free calcium concentration ([Ca2+]) measurements, which were performed as previously described Wuorela et al, 1992). The hearts were removed and weighed, and the superior mesenteric arteries carefully excised and cleaned of adherent connective tissue.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of arterial relaxation by long‐term atenolol treatment in spontaneously hypertensive rats

Kähönen¹,

Mäkynen²,

Arvola³

et al. 1994

British J Pharmacology

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1 The effects of long-term atenolol (25 mg kg-' day-') therapy on arterial function were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The 14-week treatment attenuated the increase in blood pressure by approximately 30 mmHg in SHR, but did not affect blood pressure in WKY rats. 2 Responses of mesenteric arterial rings in vitro were examined at the end of the study. The relaxation to acetylcholine was similar in WKY rats and atenolol-treated SHR and more pronounced than in untreated SHR, whereas the relaxation to the nitric oxide donor 3-morpholinosydnonimine (SIN-1) was comparable in all study groups. Moreover, after maximal relaxations to acetylcholine, marked recontractions developed in untreated SHR but not in the other groups. Vasorelaxation to isoprenaline was also attenuated in SHR and was moderately improved by the atenolol therapy. 3 Arterial relaxation induced by return of potassium to the organ bath upon precontractions elicited by potassium-free solution were used to evaluate vascular smooth muscle Na+,K+-ATPase. The rate of potassium relaxation was fastest in WKY rats and was also faster in atenolol-treated than in untreated SHR. 4 The ability of vascular smooth muscle to sequester calcium was evaluated by eliciting responses to caffeine or noradrenaline after loading periods in different organ bath calcium concentrations. The subsequent contractions were lower in untreated SHR than in WKY rats, and augmented in SHR by the atenolol treatment. 5Smooth muscle contractions to noradrenaline were comparable in SHR and WKY rats, while atenolol treatment slightly increased the maximal response to this agonist in SHR. Responses to potassium chloride were not affected by atenolol and contractions following cumulative re-addition of calcium to the organ bath after precontraction with potassium chloride and noradrenaline in calciumfree solution were comparable in all study groups. 6 In conclusion, the moderate antihypertensive effect of atenolol in SHR was accompanied by enhancement of P-adrenoceptor-mediated and normalization of endothelium-dependent arterial relaxation. Furthermore, ability to sequester calcium into cellular stores, and function of Na+,K+-ATPase were augmented in vascular smooth muscle. Therefore, the present results suggest that the long-term blood pressure-lowering action of atenolol in this type of genetic hypertension is accompanied by improved arterial relaxation and normalization of endothelial function.

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High calcium diet augments vascular potassium relaxation in hypertensive rats.

Cited by 28 publications

References 32 publications

Dietary calcium and blood pressure in experimental models of hypertension. A review.

Dietary calcium and blood pressure in experimental models of hypertension. A review.

High blood pressure-lowering and vasoprotective effects of milk products in experimental hypertension

Enhancement of arterial relaxation by long‐term atenolol treatment in spontaneously hypertensive rats

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