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DOI 10.1097/hjh.0b013e3280112cf6

Медицинская библиотека · Journal of hypertension · 2007

Total peripheral resistance responsiveness during the development of secondary renal hypertension in dogs.

Anderson Warwick P, Shweta Amany, Evans Roger G, Edgley Amanda J, Gao Yi

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVE

To determine whether the responses of total peripheral resistance and arterial pressure to vasoconstrictor agents are amplified as renovascular hypertension develops in dogs.

METHODS

After baseline measurements, the effects of renal artery stenosis (1K, 1C hypertension) were studied in groups of untreated and enalapril-treated dogs early (1-3 weeks) and later (4-6 weeks) as the hypertension developed. Both resting and open-loop haemodynamic measurements were made and the effects of acute intravenous infusions of vasopressin (0.25, 0.5 and 1.25 ng/kg per min) and phenylephrine (0.125, 0.25 and 0.50 microg/kg per min on arterial pressure, cardiac output and calculated total peripheral resistance responses were measured.

RESULTS

Renal artery stenosis induced an increase in arterial blood pressure in both groups of dogs, with similar changes in haemodynamics also observed in open-loop conditions. The slopes of arterial pressure and peripheral resistance responses to vasopressin and phenylephrine were not significantly changed in early or late hypertension, in either the untreated or enalapril-treated groups.

CONCLUSIONS

Hypertension from renal artery stenosis in dogs was due to nonautonomic, nonangiotensin II mechanisms. There was no evidence of vascular amplification of the effects of vasoconstrictor agents, indicating that this did not play a role in the development of hypertension.

Для цитирования: Anderson Warwick P, Shweta Amany, Evans Roger G, Edgley Amanda J, Gao Yi. Total peripheral resistance responsiveness during the development of secondary renal hypertension in dogs.. Journal of hypertension. 2007. DOI: 10.1097/hjh.0b013e3280112cf6.

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