Renin secretion from dispersed kidney cortex cells : role of nitric oxide, osmotic forces and the effects of Diabetes mellitus and acute renal failure
Renin secretion from dispersed kidney cortex cells : role of nitric oxide, osmotic forces and the effects of Diabetes mellitus and acute renal failure
The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure and fluid balance. Renin release is dependent on a multitude of haemodynamic, chemical, endocrine and nervous factors. The experiments described in this thesis investigating the intracellular control of renin secretion were carried out using a superfused dispersed renal cortical cell preparation. This is a highly sensitive preparation which is free from haemodynamic and tubular influences, unlike some of the other in vitro preparations currently in use. Preliminary studies showed sensitivity to stimulation by catecholamines to be high. The preparation was therefore used to investigate the effects of diabetes mellitus and acute renal failure on renin secretion. The possible roles of nitric oxide (NO) and osmotic forces in the intracellular control of renin release were also investigated.
Rats with type I chemically-induced and hereditary diabetes mellitus did not show altered sensitivity to isoprenaline or diltiazem, suggesting a cellular level change in renin secretion control does not contribute to diabetic hypertension and nephropathy. However, type II diabetic rats were more sensitive to isoprenaline, but not diltiazem, suggesting that altered juxtaglomerular cell function may contribute to the renal and circulatory changes in type II diabetes.
Rats with uranyl nitrate-induced acute renal failure also did not show altered sensitivity to isoprenaline or diltiazem, despite the tubular damage induced by this disease model. This suggests that alterations in renin secretion control at the cellular level do not contribute pathogenically to the development of hypertension in acute renal failure.
The substrate for NO synthase, L-arginine, acetylcholine and bradykinin, both of which have receptors on the endothelial cells, the nitrovasodilator sodium nitroprusside and the cyclic GMP analogue, 8-bromo cyclic GMP, all stimulated renin secretion. The NO synthase inhibitor L-NAME blocked responses to L-arginine, but not to sodium nitroprusside or 8-bromo cyclic GMP, whereas the guanylate cyclase inhibitor methylene blue blocked responses to L-arginine acetylcholine, bradykinin and sodium nitroprusside.
University of Southampton
D'Aloia, Marie-Ann Emmanuelle
5f95431d-a4e3-44cc-947a-aa0efb335588
1993
D'Aloia, Marie-Ann Emmanuelle
5f95431d-a4e3-44cc-947a-aa0efb335588
D'Aloia, Marie-Ann Emmanuelle
(1993)
Renin secretion from dispersed kidney cortex cells : role of nitric oxide, osmotic forces and the effects of Diabetes mellitus and acute renal failure.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure and fluid balance. Renin release is dependent on a multitude of haemodynamic, chemical, endocrine and nervous factors. The experiments described in this thesis investigating the intracellular control of renin secretion were carried out using a superfused dispersed renal cortical cell preparation. This is a highly sensitive preparation which is free from haemodynamic and tubular influences, unlike some of the other in vitro preparations currently in use. Preliminary studies showed sensitivity to stimulation by catecholamines to be high. The preparation was therefore used to investigate the effects of diabetes mellitus and acute renal failure on renin secretion. The possible roles of nitric oxide (NO) and osmotic forces in the intracellular control of renin release were also investigated.
Rats with type I chemically-induced and hereditary diabetes mellitus did not show altered sensitivity to isoprenaline or diltiazem, suggesting a cellular level change in renin secretion control does not contribute to diabetic hypertension and nephropathy. However, type II diabetic rats were more sensitive to isoprenaline, but not diltiazem, suggesting that altered juxtaglomerular cell function may contribute to the renal and circulatory changes in type II diabetes.
Rats with uranyl nitrate-induced acute renal failure also did not show altered sensitivity to isoprenaline or diltiazem, despite the tubular damage induced by this disease model. This suggests that alterations in renin secretion control at the cellular level do not contribute pathogenically to the development of hypertension in acute renal failure.
The substrate for NO synthase, L-arginine, acetylcholine and bradykinin, both of which have receptors on the endothelial cells, the nitrovasodilator sodium nitroprusside and the cyclic GMP analogue, 8-bromo cyclic GMP, all stimulated renin secretion. The NO synthase inhibitor L-NAME blocked responses to L-arginine, but not to sodium nitroprusside or 8-bromo cyclic GMP, whereas the guanylate cyclase inhibitor methylene blue blocked responses to L-arginine acetylcholine, bradykinin and sodium nitroprusside.
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Published date: 1993
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Local EPrints ID: 462834
URI: http://eprints.soton.ac.uk/id/eprint/462834
PURE UUID: 5d115fcd-b75c-4814-abfe-171b2dd1b8f3
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Date deposited: 04 Jul 2022 20:13
Last modified: 23 Jul 2022 01:08
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Author:
Marie-Ann Emmanuelle D'Aloia
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