Effects of ace inhibitor (captopril) on canine systemic capacitance vessels: A study with the measurement of mean circulatory pressure

T. Sahashi, H. Ito, K. Nagata, I. Hirose, H. Wada, K. Takai, S. Hirakawa

Research output: Contribution to journalArticlepeer-review

Abstract

Captopril (CAP), recently developed as an antihypertensive drug, is classified as a balanced vasodilator, and it has been used as one of the vasodilator drugs in the treatment of ''refractory'' congestive heart failure. The vasodilator action of CAP on the systemic resistance vessels has been established. However, the vasodilator action of CAP on the systemic capacitance vessels has not been fully clarified. We investigated the vasodilator effects of CAP on the systemic capacitance and resistance vessels from changes in the mean circulatory pressure (MCP) and the total peripheral resistance (TPR), respectively in response to intravenous CAP (1mg/kg) in open-chest dogs, anesthetized with intravenous pentobarbital, breathing artifically with a respirator. Thus, vasodilator actions of CAP on the systemic resistance and capacitance vessels were compared. The experiments were performed on 5 groups of dogs; (1) group of untreated dogs (n=8), (2) TSA group in which the dogs were subjected to total spinal anesthesia (TSA) followed by a continuous intravenous infusion of epinephrine to maintain the mean blood pressure (MBP) at about 100 mmHg (n=8), (3) AG II group in which MBP was previously elevated by about 30 mmHg above the basal level with a continous intravenous infusion of angiotensin II (AG II) (n=8), (4) NE group in which MBP was previously elevated by about 30 mmHg above the basal level with a continuous intravenous infusion of norepinephrine (NE) (n=8), (5) IND + APR + AG II group in which MBP was elevated by about 30 mmHg with a continuous intravenous infusion of AG II after pretreatment with indomethacin (IND, 5mg/kg, i.v.), a prostaglandin synthesis inhibitor, and aprotinin (APR, 25,000 K. I. E./ .body), kallikrein inhibitor (n=8). We measured the percentage decrease in MCP (% ΔMCP) and TPR (%ΔTPR) occurring in response to CAP in the above 5 groups to estimate the probable mechanisms of the acute vasodilator effects of CAP.

Original languageEnglish
Pages (from-to)1011-1023
Number of pages13
JournalActa Scholae Medicinalis Universitatis in Gifu
Volume37
Issue number6
Publication statusPublished - 1989
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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