title: Pressor systems involved in the maintenance of arterial pressure after lesions of the rostral ventrolateral medulla.
abstract: The current study examined three pressor systems which might support mean arterial pressure (MAP) after lesions of the rostral ventrolateral medulla (RVLM). In two protocols, bilateral electrolytic lesions or sham lesions were placed in the RVLM of rats anesthetized with sodium pentobarbital. In the first protocol, the following drugs were given sequentially after placement of the lesions: captopril (5 mg/kg) and d-pentamethylene methylated tyrosine (30 micrograms/kg), a vascular arginine-vasopressin antagonist (AVPX). A final procedure consisted of spinal-cord transection. The second protocol was identical to the first except that the order of drug administration was reversed. In the first protocol, RVLM lesions caused a slight, but statistically significant, decrease in MAP from 118 +/- 3 mmHg to 103 +/- 5 mmHg. After captopril and AVPX, MAP further decreased to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. The MAP fell to 38 +/- 2 mmHg after spinal-cord transection. In the sham-lesion group, MAP rose slightly from 127 +/- 6 mmHg to 134 +/- 7 mmHg after placement of the sham lesions. A significant reduction in MAP was not seen until after administration of AVPX, which decreased MAP to 103 +/- 6 mmHg. Spinal-cord transection substantially lowered MAP to 36 +/- 4 mmHg. In the second protocol, RVLM lesions had no effect on MAP. Administration of AVPX had little effect on MAP (before: 117 +/- 5 mmHg; after: 102 +/- 7 mmHg). In contrast, sequential administration of captopril substantially decreased MAP to 55 +/- 5 mmHg. Spinal cord transection lowered MAP to 33 +/- 1 mmHg. A decrease in MAP in the companion sham-lesion group was not seen until after administration of captopril (before: 109 +/- 8 mmHg; after: 89 +/- 11 mmHg). The greatest fall in MAP followed spinal cord transection (to 39 +/- 6 mmHg). These results demonstrate normotension after RVLM lesions despite a marked reduction in sympathetic vasomotor activity. They also indicate that, after RVLM lesions, arterial pressure is maintained mainly by activity of the renin-angiotensin system and by AVP secretion.
authors.affiliation: Department of Pharmacology, University of Texas Health Science Center, San Antonio.
authors.forename: K L
authors.initials: KL
authors.lastname: Cochrane
authors.forename: M A
authors.initials: MA
authors.lastname: Nathan
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D051381:Rats; D017483:Receptors, Vasopressin / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000502:physiology; D013116:Spinal Cord / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
chemical_list: D017483:Receptors, Vasopressin; D001127:Arginine Vasopressin; D002216:Captopril