Structural and functional changes in vascular resistance and reactivity in the deoxycorticosterone acetate (DOCA)-hypertensive pig.
The development of altered vascular resistance and reactivity was characterized in a new model of hypertension, the deoxycorticosterone acetate (DOCA)-hypertensive pig. Terminal hindlimb perfusion studies were carried out on pigs (young uninephrectomized males) approximately 50 days after implantation of DOCA or control Silastic strips. Data from these studies showed that hypertensive vascular beds (n = 5) had significantly greater (P less than 0.005) resistances than controls (n = 9) both before and after maximla vasodilation with papaverine. In response to intra-arterial injections of norepinephrine, hypertensive pigs (n = 8) demonstrated shifts in the dose-response curves to the left and lower vasoconstrictor thresholds than controls (n = 10). Preliminary observations have been made on the effects of "protecting" the hindlimb vascular bed from the increased arterial pressure by external iliac artery ligation. Although this "protection" was incomplete it prevented the development of structurally based changes in resistance and reactivity, but did not prevent the development of increased vascular smooth muscle sensitivity. It is concluded that resistance vessels in the DOCA-hypertensive pig demonstrate changes in both structure and function; structural changes do not occur when the vessels are partially protected from the increased wall stress but this does not prevent the increase in sensitivity. The structural component of resistance makes a greater contribution to the overall increase in resistance in this stage of hypertension than does the smooth muscle contraction; however, since the structural change is secondary to the increase in arterial pressure, it cannot initiate the hypertension.[1]References
- Structural and functional changes in vascular resistance and reactivity in the deoxycorticosterone acetate (DOCA)-hypertensive pig. Berecek, K.H., Bohr, D.F. Circ. Res. (1977) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg