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  • Title: Contribution of stenosis resistance to the rise in total peripheral resistance during experimental renal hypertension in conscious dogs.
    Author: Anderson WP, Korner PI, Angus JA, Johnston CI.
    Journal: Clin Sci (Lond); 1981 Dec; 61(6):663-70. PubMed ID: 7028365.
    Abstract:
    1. Mild, moderate and severe renal artery stenosis was induced by uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, following by a return to control values 24 h after deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. In moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. In these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. In mild stenosis the changes in both cardiac output and total peripheral resistance was variable and not statistically significant. In this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. In all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of non-renal beds.
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