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Published on: January 24, 2012
Haemodynamic mechanisms of corticotropin (ACTH)-induced hypertension in the rat
1Department of Medicine, The St George Hospital, University of New South Wales, Sydney, Australia.
Insights
Corticotropin (ACTH)-induced hypertension in rats involves increased renal vascular resistance (RVR), not cardiac output or total peripheral resistance. Ramipril prevented both hypertension and increased RVR, suggesting RVR
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Endocrinology
Background:
- Corticotropin (ACTH) is known to induce hypertension.
- The precise mechanisms, including the roles of cardiac output and vascular resistances, in ACTH-induced hypertension remain incompletely understood.
Purpose of the Study:
- To investigate the contribution of cardiac output (CO), systemic vascular resistance (SVR), and regional vascular resistances to ACTH-induced hypertension in a rat model.
- To evaluate the effects of specific pharmacological interventions on these hemodynamic parameters during ACTH administration.
Main Methods:
- Male Sprague-Dawley rats were treated with ACTH or saline (sham) for 10 days.
- Groups received either atenolol (beta-blocker), minoxidil (vasodilator), or ramipril (ACE inhibitor) in combination with ACTH or sham treatment.
- Hemodynamic parameters including blood pressure, cardiac output, and regional blood flows (renal, mesenteric, hindquarter) were measured.
Main Results:
- ACTH treatment significantly increased blood pressure, cardiac output, and renal vascular resistance (RVR), but not total peripheral resistance (TPR).
- Atenolol blocked the ACTH-induced rise in CO but did not affect the blood pressure increase.
- Minoxidil reduced TPR but failed to prevent ACTH-induced hypertension or increased RVR. Ramipril attenuated both the rise in RVR and blood pressure.
Conclusions:
- The development of ACTH-induced hypertension in rats is primarily associated with an increase in renal vascular resistance, rather than changes in cardiac output or total peripheral resistance.
- Ramipril's ability to prevent both hypertension and increased RVR suggests a critical role for RVR in the pathogenesis of ACTH-induced hypertension.
Objectives:
To investigate the roles of cardiac output and systemic and regional resistances in corticotropin (ACTH)-induced hypertension in the rat
Methods:
This study consisted of three series of experiments with eight groups of male Sprague-Dawley rats (n = 132). Series 1 comprised groups 1-4, where group 1 = sham (0.9% NaCl, subcutaneous (s.c.) injection); group 2 = ACTH (0.5 mg/kg per day, s.c.); group 3 = atenolol + sham; group 4 = atenolol + ACTH treatments. Series 2 comprised groups 5 and 6, where group 5 = minoxidil + sham and group 6 = minoxidil + ACTH treatments. Series 3 comprised groups 7 and 8, where group 7 = ramipril + sham and group 8 = ramipril + ACTH treatments. Systolic blood pressure, water and food intakes, urine volume, and body weight were measured every second day. After 10 days of treatment, mean arterial blood pressure was measured by intra-arterial cannulation, and cardiac output (CO), and renal, mesenteric and hindquarter blood flows (RBF, MBF and HBF) determined using transonic small animal flowmeters.
Results:
ACTH treatment increased blood pressure (P < 0.001) with a rise in CO (P < 0.01) and renal vascular resistance (RVR, P < 0.05), but did not affect total peripheral resistance (TPR). Atenolol blocked the rise in CO without affecting the rise in blood pressure produced by ACTH treatment Minoxidil lowered TPR, but did not prevent the rise in blood pressure or renal vascular resistance. Ramipril blunted the rise in RVR and blood pressure without significantly affecting TPR.
Conclusion:
Neither preventing rise in CO nor lowering TPR altered the ACTH-induced rise in blood pressure in the rat However, both the hypertension and rise in RVR were prevented by ramipril. These data suggest that increase in RVR may play a role in the pathogenesis of ACTH-induced hypertension in the rat.
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