Key result
Intravenous NG-nitro-L-arginine dose-dependently increased mean arterial pressure (peak 53 +/- 3 mmHg at 32 mg/kg) and caused a biphasic heart rate response mediated by autonomic nerve activities.
Why the study?
Does NG-nitro-L-arginine affect mean arterial pressure and heart rate in conscious rats, and is this dependent on autonomic nerve activity?
Does NG-nitro-L-arginine affect mean arterial pressure and heart rate in conscious rats, and is this dependent on autonomic nerve activity?
L-NNA increases mean arterial pressure independently of the autonomic nervous and renin-angiotensin systems, while its biphasic heart rate response is mediated by autonomic nerve activities.
Caution against clinical use of L-NNA; leaves open translation of autonomic HR effects to human cardiovascular models.
The effects of NG-nitro-L-arginine (L-NNA) on mean arterial pressure (MAP) and heart rate (HR) were investigated in conscious rats. 2. Intravenous bolus cumulative doses of L-NNA (1-32 mg kg-1) dose-dependently increased MAP. Both mecamylamine and phentolamine increased MAP responses to L-NNA, angiotensin II and methoxamine. Propranolol, reserpine, atropine and captopril did not affect MAP response to L-NNA. 3. A significant negative correlation of HR and MAP responses to L-NNA was obtained in control rats but not in rats pretreated with reserpine or mecamylamine. Significant negative correlations also occurred in the presence of atropine, propranolol, phentolamine or captopril. 4. A single i.v. bolus dose of L-NNA (32 mg kg-1) raised MAP to a peak value of 53 +/- 3 mmHg and the effect lasted more than 2 h; the rise and recovery of MAP were accompanied by significant decrease and increase in HR, respectively. While both phentolamine and mecamylamine increased peak MAP response to L-NNA, mecamylamine abolished the biphasic HR response and phentolamine potentiated the bradycardiac component of HR. 5. Blockade of the autonomic nervous and renin-angiotensin systems did not attenuate the pressor effects of L-NNA. However, the biphasic HR response to L-NNA is mediated via modulation of autonomic nerve activities.
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Wang et al. (1991) studied this question. NG-nitro-L-arginine (L-NNA) vs. Control rats and rats pretreated with autonomic blockers was evaluated on Mean arterial pressure (MAP) and heart rate (HR). Intravenous NG-nitro-L-arginine dose-dependently increased mean arterial pressure (peak 53 +/- 3 mmHg at 32 mg/kg) and caused a biphasic heart rate response mediated by autonomic nerve activities.
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