PMID- 2434779
OWN - NLM
STAT- MEDLINE
DCOM- 19870417
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 8 Suppl 7
DP  - 1986
TI  - Differential actions of neuronal and hormonal vasopressin on blood pressure and 
      baroreceptor reflex sensitivity in rats.
PG  - S81-6
AB  - The central cardiovascular actions of arginine vasopressin (AVP) and the role of 
      this peptide in the modulation of baroreceptor reflex (BRR) sensitivity were 
      investigated in conscious, chronically instrumented rats. Intracerebroventricular 
      (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent pressor effects 
      together with increases in heart rate, splanchnic, and renal sympathetic nerve 
      activity and a reduction of mesenteric blood flow. These responses were prevented 
      by i.c.v. pretreatment with a V1-AVP receptor antagonist. Furthermore, the 
      central pressor effects of AVP were abolished by peripheral alpha-adrenoceptor 
      blockade with phentolamine. In contrast to the i.c.v. injections, intravenous 
      (i.v.) or intracarotid injections of AVP produced pressor responses accompanied 
      by bradycardia and a decrease in sympathetic nerve activity. 
      Intracerebroventricular pretreatment with a V1-AVP receptor antagonist shifted 
      the slope of the BRR curve (increases in pulse interval plotted against increases 
      in systolic blood pressure in response to i.v. methoxamine) toward higher 
      sensitivity, whereas i.v. pretreatment with a V2-AVP receptor antagonist shifted 
      the slope of the BRR curve toward lower sensitivity of the reflex. These findings 
      suggest that central (neuronal) AVP, by acting on V1-AVP receptors in the brain, 
      participates in central pressor mechanisms, activates the sympathetic nervous 
      system, and desensitizes the BRR. Conversely, circulating (hormonal) AVP can 
      sensitize the BRR by acting on V2-AVP receptors accessible from the blood. Our 
      data provide evidence pointing to a direct interaction between the neuronal and 
      the hormonal axis of the AVP system within cardiovascular control.
FAU - Unger, T
AU  - Unger T
FAU - Rohmeiss, P
AU  - Rohmeiss P
FAU - Demmert, G
AU  - Demmert G
FAU - Luft, F C
AU  - Luft FC
FAU - Ganten, D
AU  - Ganten D
FAU - Lang, R E
AU  - Lang RE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Receptors, Angiotensin)
RN  - 0 (Receptors, Vasopressin)
RN  - 11000-17-2 (Vasopressins)
RN  - 113-79-1 (Arginine Vasopressin)
SB  - IM
MH  - Animals
MH  - Arginine Vasopressin/pharmacology
MH  - Blood Pressure/*drug effects
MH  - Hemodynamics/drug effects
MH  - Injections, Intraventricular
MH  - Male
MH  - Neurons/*physiology
MH  - Pressoreceptors/*drug effects
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Receptors, Angiotensin/drug effects
MH  - Receptors, Vasopressin
MH  - Reflex/drug effects
MH  - Sympathetic Nervous System/drug effects
MH  - Vasopressins/*pharmacology
EDAT- 1986/01/01 00:00
MHDA- 1986/01/01 00:01
CRDT- 1986/01/01 00:00
PHST- 1986/01/01 00:00 [pubmed]
PHST- 1986/01/01 00:01 [medline]
PHST- 1986/01/01 00:00 [entrez]
AID - 10.1097/00005344-198600087-00016 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1986;8 Suppl 7:S81-6. doi: 
      10.1097/00005344-198600087-00016.