Cold-induced hypertension. A model of mineralocorticoid-induced hypertension.
Hypertension, tachycardia and cardiac hypertrophy develop in rats exposed to mild cold (5 degrees C, 41 degrees F) for 1 to 3 weeks. Elevation of blood pressure (BP) during cold exposure is sodium dependent, although the rats still have an elevation of BP with a minimum of NaCl in their diet. Drugs that interfere with the renin-angiotensin-aldosterone (RAA) system at various levels (propranolol, clonidine, captopril, losartan and spironolactone) are able to prevent the development of cold-induced hypertension (CIH). Plasma renin activity (PRA) increases during the first 3 weeks of exposure to cold and then gradually decreases toward control level. Increased blood pressure and dipsogenic sensitivity to administration of angiotensin II (Ang II) have been demonstrated during the first 3 weeks of exposure to cold suggesting an upregulation of Ang II receptors when PRA is elevated. Additional studies have shown greater Fos-like immunoreactivity in the diencephalon of cold-exposed compared to warm-acclimated rats after 1 hr i.v. infusion of Ang II (333 ng/kg/min). Thus, most characteristics of cold-induced hypertension mimic those of hypertension induced experimentally by chronic administration of large doses of deoxycorticosterone acetate (DOCA) and salt. The results suggest that CIH is a mineralocorticoid-induced hypertension and that various levels of the RAA system contribute.[1]References
- Cold-induced hypertension. A model of mineralocorticoid-induced hypertension. Sun, Z., Cade, J.R., Fregly, M.J. Ann. N. Y. Acad. Sci. (1997) [Pubmed]
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