Cardiovascular effects of lesions of the rostral ventrolateral medulla and the nucleus reticularis parvocellularis in rats.
This study explored the possibility that the nucleus reticularis parvocellularis (NRP) acts in concert with the rostral ventrolateral medulla (RVLM) in the maintenance of mean arterial pressure (MAP). Bilateral electrolytic or chemical lesions (kainic acid) were placed in three groups of rats anesthetized with sodium pentobarbital. In the different groups, lesions were placed only in the NRP or RVLM or in both the NRP and RVLM (NRPRVLM). Captopril (5 mg/kg, i.v.) and an arginine vasopressin antagonist (AVPX), d-pentamethylene methylated tyrosine (30 micrograms/kg, i.v.), were sequentially administered. A final procedure consisted of spinal cord transection. The RVLM lesions did not significantly alter MAP (before: 116 +/- 3 mmHg; after: 106 +/- 5 mmHg). Sequential administration of captopril and AVPX each reduced MAP to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. Spinal-cord transection lowered MAP to 38 +/- 2 mmHg. Lesions of the NRP also did not alter MAP (before: 113 +/- 4 mmHg; after: 118 +/- 5 mmHg). Captopril reduced MAP to 109 +/- 7 mmHg, AVPX had no effect, and spinal-cord transection decreased MAP to 31 +/- 3 mmHg. In contrast to the lack of effect of lesions of the RVLM or NRP on MAP, profound hypotension was observed after NRPRVLM lesions (before: 113 +/- 3 mmHg; after: 51 +/- 3 mmHg). Subsequent administration of captopril decreased MAP to 39 +/- 2 mmHg, and AVPX lowered MAP to 32 +/- 1 mmHg. Spinal-cord transection reduced MAP to 23 +/- 1 mmHg. Several conclusions can be drawn from this study. First, lesions of the RVLM do not decrease MAP because of compensation by the renin-angiotensin system and AVP secretion which is mediated by the NRP. Second, lesions of the NRP do not affect MAP because the intact RVLM can maintain sympathetic tone. Third, the profound hypotension observed after NRPRLVM lesions occurred because of the simultaneous impairment of sympathetic vasomotor activity and the neuroendocrine vasoconstrictor effects of the renin-angiotensin system and AVP secretion.
Cochrane
K L
KL
Department of Pharmacology, University of Texas Health Science Center, San Antonio.
Nathan
M A
MA
D000818:Animals; D001127:Arginine Vasopressin / Q000037:antagonists & inhibitors / Q000378:metabolism; D001794:Blood Pressure; D002216:Captopril / Q000494:pharmacology; D007022:Hypotension / Q000209:etiology; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D012084:Renin-Angiotensin System / Q000502:physiology*; D012154:Reticular Formation / Q000187:drug effects / Q000502:physiology*
D001127:Arginine Vasopressin; D002216:Captopril; D010424:Pentobarbital