Parathyroids, thyroid and development of hypertension in shr.

Schleiffer, R.; Berthelot, Alain; Pernot, F; Gairard, A.

doi:10.1253/jcj.45.1272

Cited by 25 publications

(13 citation statements)

References 25 publications

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“…13 Extreme dietary calcium deprivation was associated with increased blood pressure, 10 but firm conclusions were impossible since the concomitant secondary hyperparathyroidism and magnesium depletion also could have altered the blood pressure. 16 -" Although a high calcium diet has been associated with reduced blood pressure, 5 ' 6 -"• 18 hypercalcemia of a comparable magnitude, achieved by long-term calcium injections, did not reproduce these results. 18 More importantly, when the reduction in PO 4 balance that accompanied oral calcium loading was prevented, the antihypertensive effect was also abolished.…”

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“…6 Even if statistically established, the mechanism may not be related to the undocumented increase in calcium balance, 56 since the role of an initial natriuresis 18 and suppressed parathyroid hormone levels 16 could not be excluded by merely checking serum and urine chemistry values at 2-to 4-week intervals in these outpatient studies. 6 Evaluating the third prediction, we found that 25-day-old, prehypertensive SHR not only absorbed more calcium, similar to findings in older, adult SHR, 12 but also excreted less calcium.…”

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Evidence against the role of calcium deficiency in genetic hypertension.

Lau¹,

Gafter²,

Rydell³

et al. 1986

Hypertension

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SUMMARY Epidemiological studies suggest an association between reduced calcium uptake and hypertension, while clinical trials and rat experiments indicate a small but significant hypotensive effect with oral calcium supplements. These data imply that calcium deficiency has a role in genetic hypertension. We reasoned that if the hypothesis is correct, the hypertension should be aggravated by further reducing calcium balance but attenuated by augmenting calcium balance. We tested this hypothesis by evaluating the blood pressure response in spontaneously hypertensive rats (SHR) as calcium balance was decreased by dietary restriction of calcium or increased by supplementation with magnesium or la,25-dihydroxycholecalciferol (calcitriol). A low calcium diet within the physiological range did not accentuate the hypertension in SHR during the 11 weeks of treatment, even though calcium balance was reduced by half. Similar results were obtained with dietary calcium restriction in parathyroidectomized SHR, which excludes any offsetting effects of changes in parathyroid hormone levels. Conversely, 7 weeks of a high magnesium diet, which increased calcium balance without reducing PO 4 balance, did not correct the hypertension of SHR. Similarly, long-term administration of calcitriol failed to reduce the blood pressure of parathyroidectomized SHR and normotensive Wistar-Kyoto (WKY) controls, despite the presence of increased serum calcium levels comparable to those produced by oral calcium loading. Finally, external calcium balance was measured directly in 25-day-old, prehypertensive SHR. As a result of the increased calcium absorption and reduced calcium excretion, SHR retained more calcium than did the normotensive WKY, which directly refutes the existence of calcium deficiency at this normotensive stage. These data do not support the role of calcium deficiency in genetic hypertension. (Hypertension 8: 45-49, 1986) KEYWORDS • la,25-dihydroxycholecalciferol spontaneously hypertensive rats increased gut absorption * prehypertensive A LTHOUGH clinical 1 " 6 and animal 7 -10 studies / \ suggest that calcium deficiency has a role in ±. \ . genetic hypertension, a cause-and-effect relationship has not been established from epidemiological studies, 4 which did not exclude many confounding variables, or from inferences using indirect indices of calcium metabolism.

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Evidence against the role of calcium deficiency in genetic hypertension.

Lau¹,

Gafter²,

Rydell³

et al. 1986

Hypertension

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“…23 Parathyroidectomy in young genetically hypertensive rats, while keeping a normal serum calcium level, delayed the rise in systolic blood pressure for 42 weeks. 24 In humans, information on the part played by changes in calcium metabolism in the development of high blood pressure may be gained from comparison of parameters of calcium homeostasis between offspring of hypertensive parents and offspring of normotensive parents. 25 We studied indexes of calcium metabolism in 180 normotensive offspring from 121 families with two, one, or no hypertensive parents, who were recruited out of 1,642 couples participating in a Dutch population study of risk factors for cardiovascular disease.…”

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Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Hooft¹,

Grobbee²,

Frölich³

et al. 1993

Hypertension

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Several disturbances in calcium metabolism have been reported in primary hypertensive subjects. It is, however, not clear whether these alterations predate the development of hypertension or occur as a consequence of high blood pressure. We studied indexes of calcium metabolism in three groups of normotensive children with different familial predispositions for hypertension, based on parental blood pressure levels, with two, one, or no hypertensive parents. Plasma intact parathyroid hormone pressure regulation. In some hypertensive subjects, urinary excretion of magnesium may be decreased and show an inverse relation with blood pressure.16 Serum phosphate concentration is reported to be lower in hypertension and negatively related to blood pressure. 17Besides changes in serum and urinary electrolytes, raised circulating parathyroid hormone (PTH) levels have been demonstrated in hypertensive individuals. 1318 We reported previously that plasma intact PTH is raised in young hypertensive subjects compared with normotensive subjects of similar age, suggesting that alterations in calcium metabolism may be important in the early phase of primary hypertension. 1920Discussion remains as to whether changes in calcium metabolism are causally related to the development of high blood pressure. 21 In genetically hypertensive rats, calcium supplementation during the developmental phase of hypertension diminished the blood pressure increase. 22 In another study, however, genetically hypertensive rats fed a calcium-deficient diet did not show an increased blood pressure rise compared with rats fed a normal diet. 23 Parathyroidectomy in young genetically hypertensive rats, while keeping a normal serum calcium level, delayed the rise in systolic blood pressure for 42 weeks. 24 In humans, information on the part played by changes in calcium metabolism in the development of high blood pressure may be gained from comparison of

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“…Schleiffer et al 21 observed that the parathyroid glands are necessary for the installation process of arterial hypertension. Hashimoto et al 22 suggested that the corticosteroid is essential for the development of arterial hypertension.…”

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Influence of arterial hypertension on colonic healing in rats

Ortolan¹,

Biondo-Simões

Fávero³

et al. 2012

Acta Cir. Bras.

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PURPOSE: Evaluation of colonic healing in spontaneously hypertensive rats. METHODS:Fifty male, young and inbred rats were used. Twenty-five Wistar Kyoto rats (WKY) as control and twenty-five spontaneously hypertensive rats (SHR) as an experimental group. Colotomy and bowel suture at 2.5 cm from the peritoneal reflection were performed. All animals were allocated randomly into sub-groups for review at the third, seventh and fourteenth days after surgery.We evaluated the concentration of angiotensin II, the burst pressure, epithelialization, the organization of the tunics of the bowel wall, inflammatory response and collagen deposition. RESULTS:The burst pressure, epithelialization, organization of the tunics and collagen deposition was not significant between groups.The inflammatory reaction was more intense in the control group on the third postoperative day (p=0.023) as the experimental group on the remaining time.CONCLUSION: Systemic arterial hypertension in rats did not influence significantly the healing process of colonic anastomoses.Key words: Wound Healing. Colon. Hypertension. Rats, Inbred SHR. RESUMO OBJETIVO:Avaliar a cicatrização colônica em ratos espontaneamente hipertensos. MÉTODOS:Cinquenta ratos machos, jovens e isogênicos. Vinte e cinco ratos da linhagem Wistar Kyoto (WKY) como controle e vinte e cinco ratos espontaneamente hipertensos (SHR) como grupo experimento. Realizou-se colotomia e colorrafia a 2,5 cm da reflexão peritoneal. Alocaram-se os animais aleatoriamente em sub-grupos para avaliação no terceiro, sétimo e décimo quarto dias de pós-operatório. Foram avaliados a concentração de angiotensina II, a resistência da anastomose à insuflação, a epitelização, a organização das túnicas da parede intestinal, a reação inflamatória e a deposição de colágeno. RESULTADOS:A avaliação da resistência da anastomose, epitelização, organização das túnicas e deposição de colágeno não foi significativa entre os grupos. A reação inflamatória foi mais intensa no grupo controle na avaliação do terceiro dia de pós-operatório (p=0,023) igualando-se ao grupo experimento nos demais tempos. CONCLUSÃO:A hipertensão arterial sistêmica, em ratos, não influenciou de forma significante no processo cicatricial de anastomoses do cólon.Descritores: Cicatrização. Cólon. Hipertensão. Ratos Endogâmicos SHR.

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Parathyroids, thyroid and development of hypertension in shr.

Cited by 25 publications

References 25 publications

Evidence against the role of calcium deficiency in genetic hypertension.

Evidence against the role of calcium deficiency in genetic hypertension.

Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Influence of arterial hypertension on colonic healing in rats

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