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Biomedical subjects

A Gairard

Publications and source records attributed to A Gairard.

At least 55 records · Page 3Linked to original sources
PubMed1984

[Distribution of various sites of hormonal action between microvessels, glomeruli and tubules isolated from the renal cortex of rabbits].

Collagenase dispersion of rabbit kidney cortex followed by centrifugation on discontinuous sucrose gradient, allowed the simultaneous obtention of microvascular, glomerular and tubular fractions. Microscopic studies and the measurements of cellular renin activity and the muscle-specific-enzyme creatine kinase showed that these vessels were arteriolar in nature and that they contained the preglomerular arterioles. The glomerular or tubular contamination rates were assessed by means of enzymatic markers. AVP stimulated only the tubular fraction whether GTP was present or not. In the absence of GTP, beta-isoproterenol stimulated only the tubular enzyme while in the presence of GTP, the microvascular and especially the glomerular AC were also stimulated. GTP enhanced considerably the microvascular response to bPTH-(1-34) while, in the glomeruli and tubules the effects of GTP and hormones were only additive. The possible physiological significance of these results are discussed.

Animals↗
PubMed1983

Influence of the thyroid and parathyroid glands on magnesium metabolism during mineralocorticoid treatment (DOCA + NaCl) in the rat.

The aim of the study was to investigate changes in the magnesium balance in DOCA + NaCl (S)-treated rats and the role of the parathyroid and thyroid glands in these changes during such treatment. A large loss of magnesium in the urine is observed during the onset of DOCA + S treatment, but the magnesium balance was higher after 3 weeks of treatment than in normal untreated rats. DOCA + S treatment provoked the same magnesium losses in the urine of rats without a parathyroid gland and without a thyroid gland. However, the magnesium balance was higher in rats still possessing their thyroid gland. Thus, it appears that the thyroid gland is necessary to provoke a gain in the magnesium balance during mineralocorticoid treatment.

Animals↗
PubMed1983

[The calcium dietary level modulates the development of genetic hypertension in rats].

In young male rat (Okamoto strain) hypertension develops more rapidly with a low calcium diet (0,03 per cent) and more slowly with a high calcium diet (1,2 per cent). Moreover hypertensive levels are slightly but statistically lessened after 9 months of high calcium diet. It appears that dietary calcium modulates development of genetic hypertension in the Rat.

Animal Feed↗
PubMed1983

Effect of parathyroidectomy on Sodium metabolism in DOCA-NaCl treated and spontaneously hypertensive rats.

Parathyroidectomy (PTX) lessens hypertension if performed on young SHR, and on Sprague-Dawley rats, one week before DOCA + NaCl treatment. PTX also increases diuresis and possibly sodium excretion. In this work, sodium balance was investigated during the onset of hypertension, since in SHR and DOCA + NaCl rats, sodium metabolism is related to the level of hypertension. Results show that sodium excretion is enhanced in PTX-DOCA rats immediately after DOCA treatment but lowered in PTX-SHR for 11 weeks. Nevertheless after PTX, sodium balance remains unchanged throughout the experiment. It appears that PTX does not lessen hypertensive development in both models via a decreased sodium balance.

Animals↗
PubMed1982

Parathyroidectomy significantly decreases hypertension in spontaneously hypertensive and deoxycorticosterone plus saline treated rats.

In male Sprague--Dawley rats, hypertensive development was diminished for 10 weeks when parathyroidectomy (PTX) was performed 1 week before deoxycorticosterone plus saline (DOCA + NaCl) treatment. In young spontaneously hypertensive male rats (SHR, Okamoto strain) parathyroidectomy performed after weaning lessened hypertensive levels and lowered heart rate for 24 weeks. When mineralocorticoid or genetic hypertension was established, parathyroidectomy did not significantly change blood pressure levels. High dietary calcium in PTX--SHR rats reestablished normal serum calcium but not systolic blood pressure to the level of sham SHR. From our present and previously reported results, it appears that the parathyroid gland is necessary for the total development of hypertension in both models.

Aging↗
PubMed1981

Parathyroids, thyroid and development of hypertension in SHR.

Parathyroid glands play a significant role in the development of hypertension in spontaneously hypertensive rat (SHR), like in deoxycorticosterone acetate (DOCA) + NaCl model. Parathyroidectomy (PTX) performed after weaning delayed systolic blood pressure (SBP) increase and slowed heart rate (HR) in SHR for 42 weeks. These changes could not be attributed to decrease of serum calcium in PTX animals since supplementation of calcium, rendering serum calcium normal, did not reestablish SBP and HR to those of sham SHR. Moreover, in the thyroparathyroidectomized (TPTX) animals SBP and HR were increased by autotransplantation of parathyroids. When hypertension was established (week 15), PTX produced no more changes on cardiovascular parameters measured. These data clearly indicate that independent of thyroidectomy, PTX leads to a lesser degree of hypertension in young SHR, but was without effect on established hypertension. In conclusion, parathyroid glands are required for total development of the hypertensive process in SHR.

Animals↗
PubMed1980

Parathyroid hormone- and deoxycorticosterone acetate-induced hypertension in the rat.

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

Animals↗
PubMed1980

Relation between calcium and cardiovascular reactivity in mineralocorticoid-induced hypertension in the rat.

1 Previous work has shown that parathyroidectomy (PTX) decreases cardiovascular reactivity to noradrenaline in Sprague-Dawley rats with mineralocorticoid-induced (D) hypertension. 2. In order to explain this diminution of cardiovascular reactivity, we studied in vivo the influence of serum calcium levels on the cardiac and vascular response to noradrenaline (500 ng/kg). We used rats with or without parathyroids but fed a standard or a high-calcium (+Ca) diet that re-established a serum calcium level of about 100 mg/l. Work was performed in vagotomized, anaesthetized rats after ganglionic blockage with pentolinium and atropine sulphate. 3 Cardiac output was unchanged in all the experimental groups after 11 weeks of mineralocorticoid treatment. The enhancing effect of noradrenaline was not modified. 4. Since a serum calcium level of about 100 mg/l was sufficient to re-establish vascular reactivity to exogenous noradrenaline in the PTX-D rats, parathyroid hormone was not necessary. 5 The total and lanthanum-resistant calcium fractions of the walls of the aorta were reduced in the PTX-D rats. When serum calcium levels were re-established at about 100 mg/l, there was no difference between PTX-D and D rats. 6 It is postulated that the decreased storage of calcium in vascular smooth muscle cells of PTX-D rats depresses the vascular effect of noradrenaline.

Animals↗
PubMed1980

[Parathyroidectomy and calcium exchange in cardiovascular tissue in the SHR rat].

Previous work has shown that parathyroidectomy lessens hypertension if performed on young SHR (5-6 weeks of age). In this work, ionic changes (Na+, K+, Ca2+, Mg2+) were studied in heart and aorta during a chronic experimentation. In the heart, atria and ventricle, Ca2+ content was significantly diminished, 15 days after parathyroidectomy. Nevertheless after 8 months, this difference did not remain. A correlation between Ca2+ content and heart rate (lessened immediately after parathyroidectomy) is suggested. In the aorta, parathyroidectomy did not change Na+, K+, Ca2+ and Mg2+ content after 15 days. At the opposite Mg2+ content was significantly lessened after 8 months (-33 p. 100, p less than 0,001). Calcium content in the Lanthanum Resistant Fraction was also depressed significantly at this time. Variations in heart and aorta ionic contents are discussed in relation with hypertensive development.

Animals↗
PubMed1980

Effect of DOCA-saline treatment on calcium metabolism in the rat.

This study aims to investigate changes in the calcium balance in DOCA-saline treated rats and the effect of parathyroidectomy on these changes during such treatment. However, even with this large loss in calcium, the calcium balance was higher after 2 weeks of treatment than in normal untreated rats. The DOCA-saline treatment provoked greater in normal rats. But the calcium balance became negative after 2 weeks of treatment. Thus, it appears that the presence of the parathyroid gland is necessary to provoke a gain in the calcium balance during mineralocorticoid treatment.

Animals↗
PubMed1979

Action of parathyroid extract on arterial blood pressure and on contraction and 45Ca exchange in isolated aorta of the rat.

The acute effects of parathyroid extract (PTE) on the cardiovascular system were the object of the study. PTE injected at concentrations of 10--100 U USP/kg into conscious rats induced a rapid, transitory fall in systolic blood pressure and a decrease in the total peripheral resistance. Since the cardiac output was unchanged, PTE must act on vascular smooth muscle. In vitro, PTE (2--16 U USP/ml) inhibited the tonic phase (which requires the presence of extracellular calcium) of the contraction of the thoracic aorta in response to phenylephrine or noradrenaline. 45Ca fluxes in the isolated aorta, measured by the lanthanum method, changed in the presence of a high concentration of PTE (1.0 U USP/ml). After 2 min, the influx was lowered and the efflux was enhanced. These effects may have been specific, since they did not appear when PTE had been previously inactivated. Our results suggest that the vasodilator effect of PTE in the rat is due to an action on Ca exchange in vascular smooth muscle.

Animals↗
PubMed1979

[The parathyroids and desoxycorticosterone acetate induced arterial hypertension in the rat].

We studied the importance of parathyroids in the development of mineralocorticoid hypertension in male Sprague-Dawley rats. Ablation of the parathyroids 1 week before deoxycorticosterone acetate (DOCA) + NaCl administration prevented development of hypertension (for 1 year). But ablation of parathyroids 2 weeks after the start of treatment has no effect on the development of arterial hypertension. Autotransplantation of parathyroids in thyroidectomized rats caused a recurrence of mineralocorticoid hypertension, which was completed after DL-thyroxine supplementation: blood pressure levels were nearly the same as in DOCA sham rats. We conclude that parathyroid glands favor the establishment of mineralocorticoid hypertension in the rat. These results raise the question of the mechanism of action of parathyroid hormone in the hypertensive process.

Animals↗
PubMed1978

Effect of parathyroidectomy on cardiovascular reactivity in rats with mineralocorticoid-induced hypertension.

Previous work has shown that parathyroidectomy protected Sprague-Dawley rats against mineralocorticoid hypertension. 2 In order to explain this protection, we studied vascular reactivity to noradrenaline and angiotensin II in several groups of rats with and without their parathyroid and thyroid glands. Work was performed in vagotomized, anaesthetized rats after ganglionic blockade with pentolinium, and atropine sulphate. 3 The reactivity to noradrenaline was significantly lower in parathyroidectomized rats, especially at the beginning of mineralocorticoid treatment. 4 Autotransplantation of parathyroid glands in thyroparathyroidectomized rats re-established normal cardiovascular reactivity and development of hypertension. 5 Cardiovascular reactivity to angiotensin II was not affected in parathyroidectomized rats and was lowered in thyroparathyroidectomized thyroxine-treated rats.

Angiotensin II↗
PubMed1978

Increase in urinary excretion of phosphates, hydroxyproline, and cAMP during acetate desoxycorticosterone + saline treatment in the rat.

We investigated the urinary excretion of phosphates, hydroxyproline, and cAMP in rats treated with desoxycorticosterone acetate (DOCA) associated with a hypersaline diet. We measured the three substances in groups with or without parathyroid or thyroid glands, or both. Urinary phosphate excretion increased greatly during the first weeks of treatment in normal rats and in rats autografted with parathyroids and lacking thyroid, and increased slightly in the groups without parathyroids. Hydroxyproline and cAMP had the same pattern; their excretion was greatest during week 2 of treatment in all groups, but these phenomena were more intense in animals with parathyroids. These fact support the conclusion that the parathyroid glands are stimulated during the start of mineralocorticoid-saline treatment.

Animals↗