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

Warwick Peter Anderson, Amany Abdelkader, Roger George Evans, Amanda Jane Edgley, Yi Gao

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)

Abstract

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 mug/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.
Original languageEnglish
Pages (from-to)649 - 662
Number of pages14
JournalJournal of Hypertension
Volume25
Issue number3
Publication statusPublished - 2007

Cite this

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title = "Total peripheral resistance responsiveness during the development of secondary renal hypertension in dogs",
abstract = "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 mug/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.",
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Total peripheral resistance responsiveness during the development of secondary renal hypertension in dogs. / Anderson, Warwick Peter; Abdelkader, Amany; Evans, Roger George; Edgley, Amanda Jane; Gao, Yi.

In: Journal of Hypertension, Vol. 25, No. 3, 2007, p. 649 - 662.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Total peripheral resistance responsiveness during the development of secondary renal hypertension in dogs

AU - Anderson, Warwick Peter

AU - Abdelkader, Amany

AU - Evans, Roger George

AU - Edgley, Amanda Jane

AU - Gao, Yi

PY - 2007

Y1 - 2007

N2 - 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 mug/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.

AB - 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 mug/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.

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