March 1, 1992AJP Endocrinology and Metabolism
Hypertension in insulin-resistant Zucker obese rats is independent of sympathetic neural support
Population
6- to 8-wk-old male Zucker obese rats and their lean controls (n = 10/group)
Comparison
Ganglionic blockade with Ecolid and graded… vs Lean controls
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Hypothesis-generating for vascular mechanisms in obese hypertension; leaves open relevance to human insulin-resistant states.
Key Points
- To determine whether hypertension in insulin-resistant Zucker obese rats depends on elevated sympathetic neural activity or enhanced vascular reactivity.
- Assessed 6- to 8-week-old male Zucker obese rats and lean control rats (n = 10 per group).
- Recorded intra-arterial blood pressure before and during ganglionic blockade induced by chlorisondamine chloride (Ecolid).
- Evaluated pressor responses to graded intravenous doses of angiotensin II and norepinephrine during ganglionic blockade.
- Obese rats exhibited baseline hypertension compared to lean controls (P < 0.001), and elevated blood pressure persisted during ganglionic blockade (P < 0.005).
- Obese rats demonstrated significantly greater pressor sensitivity to both angiotensin II and norepinephrine during ganglionic blockade than lean controls (P < 0.01).
Structured PICO
P
Population
6- to 8-wk-old male Zucker obese rats and their lean controls (n = 10/group)
I
Intervention
Ganglionic blockade with Ecolid (chlorisondamine chloride) and graded intravenous injections of angiotensin II and norepinephrine
C
Comparator
Lean controls
O
Outcome
Intra-arterial blood pressure responsessurrogate
In insulin-resistant Zucker obese rats, hypertension is driven by enhanced vascular pressor sensitivity rather than increased sympathetic neural activity.
Cite This Study
Zemel et al. (1992) studied this question.