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Effect of antihypertensive treatment and N omega-nitro-L-arginine methyl ester on cardiovascular structure in deoxycorticosterone acetate-salt hypertensive rats.
J Hypertens. 1996 Nov; 14(11):1331-9.JH

Abstract

BACKGROUND

Deoxycorticosterone acetate (DOCA)-salt hypertensive rats exhibit a very severe degree of cardiovascular hypertrophy, which may in part be mediated by overexpression of the endothelin-1 gene.

OBJECTIVE

To examine the effects of the angiotensin I converting enzyme inhibitor cilazapril and of the calcium channel antagonist mibefradil, both of which may affect potential mechanisms responsible for hypertrophy of cardiovascular structures, and that of the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), which may exert a paradoxical inhibitory effect on cardiovascular growth, on the severe cardiovascular hypertrophy of DOCA-salt hypertensive rats and on arterial expression of the endothelin-1 gene.

METHODS

Small-artery structure was examined on a wire myograph and endothelin-1 messenger RNA (mRNA) was quantified by Northern blot analysis.

RESULTS

Cilazapril did not affect blood pressure, cardiovascular structure or the increased abundance of endothelin mRNA of DOCA-salt hypertensive rats. Mibefradil treatment resulted in lower blood pressure, reduced cardiac hypertrophy, near-normal structure of conduit and small arteries and lower endothelin-1 mRNA abundance. L-NAME treatment resulted in higher blood pressure and increased severity of conduit artery hypertrophy, but reduced cardiac and small artery hypertrophy, and enhanced aortic endothelin-1 mRNA.

CONCLUSION

These results suggest that the renin-angiotensin system does not play a role in cardiovascular hypertrophy in DOCA-salt hypertensive rats, which is not unexpected since plasma renin is suppressed in these rats. Calcium channel blockade may interfere with mechanisms underlying vascular hypertrophy in this model via blockade of calcium entry or by reducing vascular endothelin-1 gene expression when the blood pressure is lowered. L-NAME has been shown to exert a growth-inhibitory effect on small arteries and on the heart despite increasing blood pressure, probably independently from its ability to inhibit nitric oxide synthase, the latter of which is presumably involved in the blood pressure rise induced.

Authors+Show Affiliations

MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montréal, University of Montréal, Québec, Canada.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8934362

Citation

Li, J S., et al. "Effect of Antihypertensive Treatment and N omega-nitro-L-arginine Methyl Ester On Cardiovascular Structure in Deoxycorticosterone Acetate-salt Hypertensive Rats." Journal of Hypertension, vol. 14, no. 11, 1996, pp. 1331-9.
Li JS, Sventek P, Schiffrin EL. Effect of antihypertensive treatment and N omega-nitro-L-arginine methyl ester on cardiovascular structure in deoxycorticosterone acetate-salt hypertensive rats. J Hypertens. 1996;14(11):1331-9.
Li, J. S., Sventek, P., & Schiffrin, E. L. (1996). Effect of antihypertensive treatment and N omega-nitro-L-arginine methyl ester on cardiovascular structure in deoxycorticosterone acetate-salt hypertensive rats. Journal of Hypertension, 14(11), 1331-9.
Li JS, Sventek P, Schiffrin EL. Effect of Antihypertensive Treatment and N omega-nitro-L-arginine Methyl Ester On Cardiovascular Structure in Deoxycorticosterone Acetate-salt Hypertensive Rats. J Hypertens. 1996;14(11):1331-9. PubMed PMID: 8934362.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of antihypertensive treatment and N omega-nitro-L-arginine methyl ester on cardiovascular structure in deoxycorticosterone acetate-salt hypertensive rats. AU - Li,J S, AU - Sventek,P, AU - Schiffrin,E L, PY - 1996/11/1/pubmed PY - 1996/11/1/medline PY - 1996/11/1/entrez SP - 1331 EP - 9 JF - Journal of hypertension JO - J Hypertens VL - 14 IS - 11 N2 - BACKGROUND: Deoxycorticosterone acetate (DOCA)-salt hypertensive rats exhibit a very severe degree of cardiovascular hypertrophy, which may in part be mediated by overexpression of the endothelin-1 gene. OBJECTIVE: To examine the effects of the angiotensin I converting enzyme inhibitor cilazapril and of the calcium channel antagonist mibefradil, both of which may affect potential mechanisms responsible for hypertrophy of cardiovascular structures, and that of the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), which may exert a paradoxical inhibitory effect on cardiovascular growth, on the severe cardiovascular hypertrophy of DOCA-salt hypertensive rats and on arterial expression of the endothelin-1 gene. METHODS: Small-artery structure was examined on a wire myograph and endothelin-1 messenger RNA (mRNA) was quantified by Northern blot analysis. RESULTS: Cilazapril did not affect blood pressure, cardiovascular structure or the increased abundance of endothelin mRNA of DOCA-salt hypertensive rats. Mibefradil treatment resulted in lower blood pressure, reduced cardiac hypertrophy, near-normal structure of conduit and small arteries and lower endothelin-1 mRNA abundance. L-NAME treatment resulted in higher blood pressure and increased severity of conduit artery hypertrophy, but reduced cardiac and small artery hypertrophy, and enhanced aortic endothelin-1 mRNA. CONCLUSION: These results suggest that the renin-angiotensin system does not play a role in cardiovascular hypertrophy in DOCA-salt hypertensive rats, which is not unexpected since plasma renin is suppressed in these rats. Calcium channel blockade may interfere with mechanisms underlying vascular hypertrophy in this model via blockade of calcium entry or by reducing vascular endothelin-1 gene expression when the blood pressure is lowered. L-NAME has been shown to exert a growth-inhibitory effect on small arteries and on the heart despite increasing blood pressure, probably independently from its ability to inhibit nitric oxide synthase, the latter of which is presumably involved in the blood pressure rise induced. SN - 0263-6352 UR - https://www.unboundmedicine.com/medline/citation/8934362/Effect_of_antihypertensive_treatment_and_N_omega_nitro_L_arginine_methyl_ester_on_cardiovascular_structure_in_deoxycorticosterone_acetate_salt_hypertensive_rats_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=8934362.ui DB - PRIME DP - Unbound Medicine ER -