Previous studies have reported that chronic increases in dietary salt intake enhance sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses evoked from brainstem nuclei of normotensive, salt-resistant rats. The purpose of the present study was to determine whether this sensitization results in exaggerated SNA and ABP responses during activation of various cardiovascular reflexes and also increases ABP variability (BPV). Male Sprague-Dawley rats were fed 0.1% NaCl chow (low), 0.5% NaCl chow (medium), 4.0% NaCl chow (high) for 14–17 days. Then, animals were prepared for recordings of lumbar, renal, and splanchnic SNA and ABP. The level of dietary salt intake directly correlated with the magnitude of SNA and ABP responses to electrical stimulation of sciatic afferents or intracerebroventricular infusion of 0.6M or 1.0M NaCl. Similarly, there was a direct correlation between the level of dietary salt intake and the sympathoinhibitory responses produced by acute volume expansion, stimulation of the aortic depressor nerve or cervical vagal afferents. In contrast, dietary salt intake did not affect the sympathetic and ABP responses to chemoreflex activation produced by hypoxia or hypercapnia. Chronic lesion of the anteroventral 3rd ventricle region eliminated the ability of dietary salt intake to modulate these cardiovascular reflexes. Finally, rats chronically instrumented with telemetry units indicate that increased dietary salt intake elevated BPV but not mean ABP. These findings indicate that dietary salt intake works through the forebrain hypothalamus to modulate various centrally-mediated cardiovascular reflexes and increase BPV.

Kinsman B, Cowles J, Lay J, Simmonds SS, Browning KN, Stocker SD. Osmoregulatory thirst in mice lacking the transient receptor potential vanilloid type 1 (TRPV1) and/or type 4 (TRPV4) receptor. Recent studies suggest the ability of the central nervous system to detect changes in osmolality is mediated by products of the genes encoding the transient receptor potential vanilloid-1 (TRPV1) or vanilloid-4 (TRPV4) channel. The purpose of the present study was to determine whether deletion of TRPV1 and/or TRPV4 channels altered thirst responses to cellular dehydration in mice. Injection of 0.5 or 1.0 M NaCl produced dose-dependent increases in cumulative water intakes of wild-type (WT), TRPV1 Ϫ/Ϫ , TRPV4 Ϫ/Ϫ , and TRPV1 Ϫ/Ϫ V4 Ϫ/Ϫ mice. However, there were no differences in cumulative water intakes between WT versus any other strain despite similar increases in plasma electrolytes and osmolality. Similar results were observed after injection of hypertonic mannitol. This was a consistent finding regardless of the injection route (intraperitoneal vs. subcutaneous) or timed access to water (delayed vs. immediate). There were also no differences in cumulative intakes across strains after injection of 0.15 M NaCl or during a time-controlled period (no injection). Chronic hypernatremia produced by sole access to 2% NaCl for 48 h also produced similar increases in water intake across strains. In a final set of experiments, subcutaneous injection of 0.5 M NaCl produced similar increases in the number of Fos-positive nuclei within the organum vasculosum of the lamina terminalis and median preoptic nucleus across strains but significantly smaller number in the subfornical organ of WT versus TRPV1 Ϫ/Ϫ V4 Ϫ/Ϫ mice. Collectively, these findings suggest that TRPV1 and/or TRPV4 channels are not the primary mechanism by which the central nervous system responds to cellular dehydration during hypernatremia or hyperosmolality to increase thirst. hypernatremia; water intake; organum vasculosum of the lamina terminalis; subfornical organ; cellular dehydration THE CENTRAL NERVOUS SYSTEM plays a pivotal role in body fluid homeostasis through its ability to sense changes in osmotic pressure and subsequently alter fluid intake, secretion of antidiuretic hormone, natriuresis, and sympathetic nerve activity (5,19,30,42,45,50). Physiologically, changes in extracellular osmotic pressure are typically the result of changes in the extracellular concentration of Na ϩ and/or Cl Ϫ to produce cellular dehydration. The most influential set of osmosensitive neurons is located within the forebrain lamina terminalis (5). This region of the brain contains several structures including two circumventricular organs: the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO). A number of laboratories have demonstrated that acute or chronic hypernatremia increases Fos immunoreactivity in the OVLT and SFO (21,36,40,46). Second, in vivo and in vitro electrophysiological studies have reported that acute hypernatremia or hyperosmolality i...

This study supports a style of consultation where students are actively involved in patient care as it has no adverse effects on patient satisfaction and it is the preferred participation style from the student's perspective. Doctors do not feel that active student involvement interferes with their ability to deliver healthcare except that it prolongs consultation time.