| Differential regional haemodynamic changes during mineralocorticoid hypertension. | |
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MedLine Citation:
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PMID: 16685214 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Primary aldosteronism is a cause of hypertension in up to 10% of hypertensive patients, but the mechanisms by which excess aldosterone raises arterial pressure remain unclear. OBJECTIVE: To investigate the systemic and regional haemodynamic changes during the development and maintenance of aldosterone-induced hypertension and the effect of sympathetic and vasopressin blockade. METHODS: Responses to intravenous infusion of aldosterone (10 microg/h) for 4 weeks were determined in five conscious sheep. The effects of sympathetic blockade with propranolol and phentolamine or vasopressin V1-receptor blockade with SR59049 were investigated in six further sheep infused with aldosterone. RESULTS: Aldosterone progressively increased the mean arterial pressure by 20 mmHg over 4 weeks (P < 0.001). The changes in cardiac output were variable between animals, resulting in no overall significant change. Total peripheral conductance was significantly decreased due to selective reductions in mesenteric conductance (from 6.17 +/- 0.27 to 4.46 +/- 0.15 ml/min per mmHg, P < 0.001) and iliac conductance (from 1.54 +/- 0.21 to 1.27 +/- 0.15 ml/min per mmHg, P < 0.001). In contrast, renal and coronary conductance were unchanged and renal blood flow increased from 290 +/- 17 to 350 +/- 28 ml/min (P < 0.01) and coronary blood flow from 34.7 +/- 3.0 to 44.6 +/- 2.5 ml/min (P < 0.05). These aldosterone-induced changes were not inhibited by sympathetic or vasopressin V1-receptor blockade. CONCLUSION: Excess aldosterone caused a slow progressive increase in arterial pressure, which in the long term depended on reduced total peripheral conductance. This resulted from vasoconstriction in the gut and skeletal muscle, but not the kidney. These effects were not mediated by the sympathetic nervous system or vasopressin. |
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Authors:
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Clive N May |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of hypertension Volume: 24 ISSN: 0263-6352 ISO Abbreviation: J. Hypertens. Publication Date: 2006 Jun |
Date Detail:
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Created Date: 2006-05-10 Completed Date: 2006-08-10 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: England |
Other Details:
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Languages: eng Pagination: 1137-46 Citation Subset: IM |
Affiliation:
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Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia. c.may@hfi.unimelb.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aldosterone
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blood,
physiology* Animals Cardiac Output / physiology* Coronary Circulation / physiology Female Hypertension / physiopathology* Iliac Artery / physiopathology Potassium / blood, urine Receptors, Vasopressin / antagonists & inhibitors Regional Blood Flow / physiology Renal Circulation / physiology Renin / blood Sheep Sodium / blood, urine Splanchnic Circulation / physiology* Sympatholytics / pharmacology Vasoconstriction / physiology |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Vasopressin; 0/Sympatholytics; 52-39-1/Aldosterone; 7440-09-7/Potassium; 7440-23-5/Sodium; EC 3.4.23.15/Renin |
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