Hong Zheng1, Kenichi Katsurada2, Shyam Nandi2, Yifan Li1, Kaushik P Patel3. 1. Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, SD 57069, Vermillion, USA. 2. Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA. 3. Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA. kpatel@unmc.edu.
Abstract
PURPOSE OF REVIEW: This review focuses on studies implicating forebrain neural pathways and neuromodulator systems, particularly, the nitric oxide system within the paraventricular nucleus of the hypothalamus in regulating neurohumoral drive, autonomic pathways, and fluid balance. RECENT FINDINGS: Accumulating evidence from animals with experimental models of hypertension and heart failure as well as humans with hypertension suggests that alterations in central neural pathways, particularly, within the PVN neuromodulated by neuronal nitric oxide, are involved in regulating sympathetic outflow particularly to the kidney resulting in alterations in fluid balance commonly observed in hypertension and heart failure states. The characteristics of the hypertensive and heart failure states include alterations in neuronal nitric oxide within the PVN to cause an increase in renal sympathetic nerve activity to result in sodium and fluid retention in these diseases. A comprehensive understanding of these mechanisms will enhance our ability to treat hypertensive and heart failure conditions and their cardiovascular complications more efficiently.
PURPOSE OF REVIEW: This review focuses on studies implicating forebrain neural pathways and neuromodulator systems, particularly, the nitric oxide system within the paraventricular nucleus of the hypothalamus in regulating neurohumoral drive, autonomic pathways, and fluid balance. RECENT FINDINGS: Accumulating evidence from animals with experimental models of hypertension and heart failure as well as humans with hypertension suggests that alterations in central neural pathways, particularly, within the PVN neuromodulated by neuronal nitric oxide, are involved in regulating sympathetic outflow particularly to the kidney resulting in alterations in fluid balance commonly observed in hypertension and heart failure states. The characteristics of the hypertensive and heart failure states include alterations in neuronal nitric oxide within the PVN to cause an increase in renal sympathetic nerve activity to result in sodium and fluid retention in these diseases. A comprehensive understanding of these mechanisms will enhance our ability to treat hypertensive and heart failure conditions and their cardiovascular complications more efficiently.