HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/2/R352    most recent 00489.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Moncrief, K. Articles by Kaufman, S. Search for Related Content PubMed PubMed Citation Articles by Moncrief, K. Articles by Kaufman, S.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Splenic baroreceptors control splenic afferent nerve activity

Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

Submitted 6 July 2005 ; accepted in final form 14 September 2005

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (–0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (–0.11 ± 0.15 spikes/s, n = 6 and –0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure (r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous (r = 0.371, P = 0.236, n = 12) or arterial (r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.

blood flow; splenic vein; portal hypertension; blood pressure

This article has been cited by other articles:

				R. Tiniakov and K. E. Scrogin The spleen is required for 5-HT1A receptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2009; 296(5): R1392 - R1401. [Abstract] [Full Text] [PDF]

				S. M. Hamza and S. Kaufman Effect of mesenteric vascular congestion on reflex control of renal blood flow Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2007; 293(5): R1917 - R1922. [Abstract] [Full Text] [PDF]

				K. Moncrief, S. Hamza, and S. Kaufman Splenic reflex modulation of central cardiovascular regulatory pathways Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R234 - R242. [Abstract] [Full Text] [PDF]

				H. M. Wadei, M. L. Mai, N. Ahsan, and T. A. Gonwa Hepatorenal Syndrome: Pathophysiology and Management Clin. J. Am. Soc. Nephrol., September 1, 2006; 1(5): 1066 - 1079. [Full Text] [PDF]