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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 811 records · Page 45Linked to original sources
PubMed1982

Vascular effects of parathyroid hormone (PTH).

PTH causes dose dependent transient vasodilatation in various vascular beds, specifically renal, coeliac, coronary, but not osseous. It has an acute dose-dependent hypotensive effect in the intact animal which is not mediated by alpha- or beta-adrenergic, cholinergic or histaminergic mechanisms. Aortic medial smooth muscle cells respond to PTH with an increase of cAMP, cGMP and, presumably via protein kinase, with activation of phosphorylase B kinase. The acute vasodilatory effect of PTH is antagonised by indomethacin and diclofenac as well as by ouabain, suggesting that the membrane Na-K pump and prostaglandins are involved in PTH-induced vasodilatation. Parathyroidectomy and a high calcium diet attenuate the rise of arterial pressure in experimental hypertension, pointing to some permissive effect of PTH for development hypertension. This is most likely due to long term effects of PTH on vessel wall calcium content and exchange. This chronic effect of PTH may explain the high prevalence of hypertension in patients with primary hyperparathyroidism.

Animals↗
PubMed1982

Dysfunction of the adrenergic system in phosphate depleted rats.

Plasma catecholamines and vascular response to noradrenaline were studied in phosphate depleted rats. Phosphate depletion was induced in rats by dietary phosphorus deprivation for 6 weeks. Basal plasma concentrations of noradrenaline, adrenaline and dopamine were elevated in phosphate depleted rats compared to pairfed control rats. After exposure to cold (4 degrees C, 45 min) the rise in plasma catecholamines was much more pronounced in phosphate depleted rats. In the isolated perfused rat heart, the uptake of tritiated noradrenaline was unchanged. In the isolated perfused hindlimb preparation the vascular response to noradrenaline, but not to potassium chloride and arginine-vasopressin was significantly diminished in phosphate depleted rats. It is concluded that in phosphate depletion sympathetic activity is elevated and vascular response to noradrenaline diminished.

Animals↗
PubMed1982

Diminished response of ovarian cAMP to luteinizing hormone in experimental uremia.

In prepuberal female rats with acute bilateral nephrectomy or chronic subtotal nephrectomy, the increase of ovarian cAMP concentration in response to submaximal doses of luteinizing hormone (LH 10 micrograms) and human chorionic gonadotropine (hCG 2.5 IU) was diminished (CO + 2.5 IU hCG 488 +/- 49 pmoles cAMP/mg protein; NX + 2.5 IU hCG 366 +/- 56. P less than 0.05). The cAMP response to follicle stimulating hormone (FSH) was unchanged. The abnormality was found both after administration of LH in vivo and incubation of ovaries with LH in vitro. Similarly, plasma estradiol concentrations in response to submaximal hCG stimulation were diminished. Basal cAMP concentrations and cAMP concentrations after maximal stimulation were unchanged. The defect was observed both in ovaries of untreated prepuberal rats, of pregnant mare serum (PMS)-treated rats (follicular phase) and PMS/hCG-treated rats (luteal phase). Diminished ovarian cAMP response to LH was observed both in parathyroid intact and in parathyroidectomized rats. Administration of 1,25(OH)2D3 in physiological doses (60 ng/kg) to acutely uremic rats restored diminished ovarian cAMP response to submaximal LH stimulation irrespective of parathyroid status. The effect of 1,25(OH)2D3 could not be reproduced by hypercalcemia resulting from intraperitoneal calcium injection. In vivo administration of indomethacin further diminished ovarian cAMP response in uremic animals and had no effect in control animals. Incubation of ovaries with PGE1 and PGE2 increased basal and stimulated cAMP concentrations and abolished the difference between control and uremic animals. The diminished response of ovarian cAMP content to submaximal doses of hCG was not corrected by bromocriptine (1 mg/kg) despite normalization of hyperprolactinemia. The present study shows diminished ovarian cAMP and plasma estradiol response to LH in experimental uremia. It documents a role of 1,25(OH)2D3 and prostaglandins in the genesis of this abnormality.

Alprostadil↗
PubMed1982

Haemodynamics and myocardial metabolism of phosphorus depleted dogs: effects of catecholamines and angiotensin II.

The responses of arterial pressure and myocardial contractile force (VPM) to infusion of angiotensin II, noradrenaline and orciprenaline were examined in twelve dogs during a control phase, after 30 days of dietary phosphorus deprivation and after 21 days of phosphorus repletion. In the phosphorus depletion period, animals had low skeletal and heart muscle Pi content, low magnesium, ATP and creatine phosphate in skeletal and heart muscle with no change of ADP, AMP or energy charge. In the basal state, VPM was diminished with no change of end-diastolic and systolic pressure. Infusion of angiotensin II caused a significantly smaller rise of arterial pressure (angiotensin II resistance), and the stimulatory effect of noradrenaline and orciprenaline on VPM was diminished (catecholamine resistance). These effects were reversible with Pi repletion. In phosphorus depletion, arterial concentrations were increased for lactate, unchanged for FFA and decreased for acetoacetate/beta-hydroxybutyrate. Unchanged myocardial extraction of lactate or beta-hydroxybutyrate and preserved cell Pi uptake for glycogenolysis were observed. The initial rate of uptake of calcium and concentrating ability of myocardial sarcoplasmic reticulum were unchanged.

Angiotensin II↗
PubMed1982

Effect of parathyroid hormone, calcitonin and growth hormone on cAMP content of growth cartilage in experimental uraemia.

The response of proximal tibial growth cartilage cAMP content to different hormonal stimuli, i.e. parathyroid hormone, calcitonin and somatotropic hormone was evaluated in rats with bilateral or subtotal nephrectomy. In uraemic rats, basal cAMP content of growth cartilage was unchanged. Administration of 1-34 PTH in vivo or incubation of growth cartilage with 1-34 PTH in vitro caused a significantly smaller increment of cAMP in uraemic rats (40 IU PTH in vivo: 11.4 +/- 1.01 pmol cAMP/mg protein; controls 24.0 +/- 2.55; P less than 0.001). This finding implies PTH resistance. Diminished cAMP response in uraemic animals was not changed by pretreatment with 1,25(OH)2D3 or parathyroidectomy. The increment of cAMP content of growth cartilage of uraemic animals was significantly (P less than 0.01) greater after in vivo administration of 10 IU calcitonin (46.1 +/- 4.89 pmol/mg protein; control: 29.0 +/- 3.99) or incubation of cartilage with calcitonin in vitro. This finding implies overresponsiveness to calcitonin. Neither in acute nor in chronic uraemia, STH caused a significant change of cartilage cAMP or cGMP content, but STH stimulated 3H-thymidine incorporation into chondrocytes of rats with 5 days uraemia (solvent 2.98 +/- 0.51 x 10(3) cpm per cartilage; STH 5.08 +/- 0.34; P less than 0.05) and caused significant improvement of longitudinal growth of rats with 20 days uraemia.

Animals↗
PubMed1982

Effects of long-term infusion of physiologic doses of 1-34 PTH on bone.

It has been suggested that small doses of PTH could exert an anabolic effect on bone and could be beneficial in the management of bone diseases secondary to low bone formation. The effects of 20 wk of continuous infusion of 0.05 U.kg-1.h-1 of 1-34 PTH on cellular, structural, and dynamic parameters of bone were studied in inbred beagles. This physiologic or near physiologic dose of PTH caused a small but significant rise in the concentration of serum calcium and a significant increment in the plasma concentration of 1,25(OH)2D. In addition, the sustained infusion of PTH was associated with a significant increment in volume and surface density of osteoid without a change in bone mass. Mineralization of osteoid was not altered, as evidenced by normal double tetracycline uptake and normal osteoid seam thickness. The enhanced osteoid production was not due to augmented bone formation by individual osteoblasts or basic remodeling units but rather to increased activation frequency resulting in an increased number of remodeling units. There was also augmented bone resorption at the tissue level. The data indicate that small doses of PTH do not have an anabolic effect on the skeleton because they are not associated with increased net bone formation. Rather, PTH administration is associated with an increase in coupled bone turnover.

Animals↗