PubMed Health⌕ Search

Biomedical subjects

Alan Kim Johnson

Publications and source records attributed to Alan Kim Johnson.

50 records · Page 3Linked to original sources
PubMed2002

Increased cellular activity in rat insular cortex after water and salt ingestion induced by fluid depletion.

Insular cortex (IC) receives inputs from multiple sensory systems, including taste, and from receptors that monitor body electrolyte and fluid balance and blood pressure. This work analyzed metabolic activity of IC cells after water and sodium ingestion induced by sodium depletion. Rats were injected with the diuretic furosemide (10 mg/kg body wt), followed 5 min later by injections of the angiotensin-converting enzyme inhibitor captopril (5 mg/kg body wt). After 90 min, some rats received water and 0.3 M NaCl to drink for 2 h while others did not. A third group had access to water and saline but was not depleted of fluids. All rats were killed for processing of brain tissue for Fos-immunoreactivity (Fos-ir). Nondepleted animals had weak-to-moderate levels of Fos-ir within subregions of IC. Fluid-depleted rats without fluid access had significantly increased Fos-ir in all areas of IC. Levels of Fos-ir were highest in fluid-depleted rats that drank water and sodium. Fos-ir levels were highest in anterior regions of IC and lowest in posterior regions of IC. These results implicate visceral, taste, and/or postingestional factors in the increased metabolic activity of cells in IC.

Afferent Pathways↗
PubMed2002

Thirst and salt appetite responses in young and old Brown Norway rats.

Male Brown Norway rats aged 4 mo (young) and 20 mo (old) received a series of experimental challenges to body fluid homeostasis over approximately 3 mo. Water was available for drinking in some tests, and both water and 0.3 M NaCl were available in others. The series included three episodes of extracellular fluid depletion (i.e., furosemide + 20 h of sodium restriction), two tests involving intracellular fluid depletion (i.e., hypertonic saline: 1 or 2 M NaCl at 2 ml/kg body wt sc), one test involving overnight food and fluid restriction, and testing with captopril adulteration of the drinking water (0.1 mg/ml) for several days. Old rats were significantly heavier than young rats throughout testing. Old rats drank less water and 0.3 M NaCl after sodium deprivation than young rats, in terms of absolute and body weight-adjusted intakes. Old rats drank only half as much water as young rats in response to subcutaneous hypertonic NaCl when intakes were adjusted for body weight. Old rats drank less 0.3 M NaCl than young rats after overnight food and fluid restriction when intakes were adjusted for body weight. In response to captopril adulteration of the drinking water, young rats significantly increased daily ingestion of 0.3 M NaCl when it was available as an alternative to water and significantly increased daily water intakes when only water was available, in terms of absolute and body weight-adjusted intakes. Old rats had no response to captopril treatment. These results add important new information to previous reports that aging rats have diminished thirst and near-absent salt appetite responses to regulatory challenges.

Aging↗
PubMed2002

Lesions of periventricular tissue surrounding the anteroventral third ventricle (AV3V) attenuate salivation and thermal tolerance in response to a heat stress.

The purpose of this study was to determine if ablation of the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) would reduce an animal's ability to withstand a thermal challenge. The results show that AV3V-lesion rats are less capable of withstanding a 37 degrees C heat stress and that this is, at least in part, due to a reduced salivation response.

Animals↗
PubMed2002

Olfactory bulbectomy attenuates cardiovascular sympathoexcitatory reflexes in rats.

Bilateral removal of the olfactory lobes in rats produces a number of behavioral, endocrine, and neurochemical alterations in the brain. Little is known, however, regarding the effects of this treatment on cardiovascular function and autonomic reflexes. Male Sprague-Dawley rats underwent bilateral surgical ablation of the olfactory bulbs (n = 10) or were sham operated (n = 8). After 3 wk of recovery, animals were instrumented with femoral catheters and a lumbar sympathetic nerve recording electrode. After 24 h of recovery, cardiovascular responses to arterial baroreflex manipulation, air jet stress, and smoke exposure were recorded. Olfactory bulbectomized rats demonstrated attenuated sympathoexcitatory responses to hypotension, air jet stress, and smoke exposure, as well as elevated basal blood pressure, compared with sham-operated rats. These data indicate that the integrity of the olfactory bulbs in rats is important for the elicitation of normal cardiovascular and autonomic responses to a number of evocative stimuli.

Animals↗
PubMed2002

Biological mechanisms in the relationship between depression and heart disease.

Psychological depression is shown to be associated with several aspects of coronary artery disease (CAD), including arrhythmias, myocardial infarction, heart failure and sudden death. The physiological mechanisms accounting for this association are unclear. Hypothalamic-pituitary-adrenal dysregulation, diminished heart rate variability, altered blood platelet function and noncompliance with medial treatments have been proposed as mechanisms underlying depression and cardiovascular disease. Recent evidence also suggests that reduced baroreflex sensitivity, impaired immune function, chronic fatigue and the co-morbidity of depression and anxiety may be involved in the relationship between depression and cardiovascular dysregulation. An experimental strategy using animal models for investigating underlying physiological abnormalities in depression is presented. A key to understanding the bidirectional association between depression and heart disease is to determine whether there are common changes in brain systems that are associated with these conditions. Such approaches may hold promise for advancing our understanding of the interaction between this mood disorder and CAD.

Animals↗
PubMed2002

Forebrain-mediated adaptations to myocardial infarction in the rat.

Recent studies suggest that the forebrain contributes to the circulatory derangements leading to heart failure after myocardial injury. We tested that hypothesis by examining the effect of myocardial infarction (MI) or sham MI (MI-s) on neurohumoral regulation in rats with prior anteroventral (AV) third ventricle lesion (AV3V-x) or sham lesion (AV3V-s). AV3V-s/MI rats had higher sodium intake, lower urine volume, and lower urinary sodium excretion than AV3V-s/MI-s rats. AV3V-x/MI rats had lower sodium intake and higher urine volume than AV3V-s/MI or AV3V-s/MI-s rats and urinary sodium excretion comparable to AV3V-s/MI-s rats. AV3V-x had no effect on baseline plasma renin activity (PRA). One week after MI, PRA had increased in AV3V-s but decreased in AV3V-x rats. AV3V-x reduced renal sympathetic nerve activity in MI and MI-s rats. AV3V-x improved baroreflex function in MI rats but diminished it in MI-s rats. Survival beyond 2 wk was lower in the AV3V-x/MI rats than in all other groups. These results confirm a critical role for the forebrain in the neurohumoral adjustments to MI.

Adaptation, Physiological↗
PubMed2002

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes.

Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 +/- 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.

Animals↗
PubMed2002

Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite.

Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 microg), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.

Animals↗
PubMed2002

Cardiovascular alterations and autonomic imbalance in an experimental model of depression.

Depressed patients with and without a history of cardiovascular pathology display signs, such as elevated heart rate, decreased heart rate variability, and increased physiological reactivity to environmental stressors, which may indicate a predisposition to cardiovascular disease. The specific physiological mechanisms associating depression with such altered cardiovascular parameters are presently unclear. The current study investigated cardiovascular regulation in the chronic mild stress rodent model of depression and examined the specific autonomic nervous system mechanisms underlying the responses. Sprague-Dawley rats exposed to a series of mild, unpredictable stressors over 4 wk displayed anhedonia (an essential feature of human depression), along with elevated resting heart rate, decreased heart rate variability, and exaggerated pressor and heart rate responses to air jet stress. Results obtained from experiments studying autonomic blockade suggest that cardiovascular alterations in the chronic mild stress model are mediated by elevated sympathetic tone to the heart. The present findings have implications for the study of pathophysiological links between affective disorders and cardiovascular disease.

Animals↗
PubMed2002

Sodium appetite and Fos activation in serotonergic neurons.

We evaluated serotonergic hindbrain groups of cells for their involvement in the generation and inhibition of sodium appetite. For that purpose, we analyzed the number of Fos-immunoreactive (Fos-ir) cells and double-labeled Fos-serotonin (5-HT)-ir neurons within different nuclei of the hindbrain raphe system and the area postrema (AP). Sodium depletion and sodium appetite were induced by peritoneal dialysis. Twenty-four hours after peritoneal dialysis, a 2% NaCl solution intake test was given to peritoneal dialyzed animals [PD-with access (PD-A) group] and to control dialyzed animals [CD-with access (CD-A) group]. Two additional groups of animals received either peritoneal dialysis or control dialysis but were not given access to the 2% NaCl [CD-no access (CD-NA) group or PD-no access (PD-NA) group]. The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. The PD-NA group had significantly fewer double-labeled cells along the raphe system compared with the animals in near-normal sodium balance (CD-NA and CD-A) or in the process of restoring sodium balance by consuming NaCl (PD-A). The AP of the PD-A group showed a significant increase in the number of Fos-ir and Fos-5-HT-ir cells compared with the PD-NA and CD groups. Our results suggest that serotonergic pathways with cell bodies in the AP and the raphe system are involved in the control of sodium appetite.

Animals↗
PubMedDate not supplied

Angiotensin II-induced drinking and pressor responses to central or systemic irbesartan and losartan.

Angiotensin II (ANG II) is a peptide hormone that is important for maintaining blood pressure and body fluid homeostasis. Two nonpeptide angiotensin type 1 (AT(1)) receptor antagonists, irbesartan and losartan, were compared for their antidipsogenic and antihypertensive efficacy in both normotensive and hypertensive rats. ANG II-induced drinking and pressor responses were examined following central or systemic administration of irbesartan and losartan. Both agents inhibited the drinking response to ANG II in normotensive rats. Irbesartan was more effective than losartan at inhibiting pressor responses to ANG II in normotensive and hypertensive rats. These data indicate that centrally administered irbesartan may be somewhat more effective as an AT(1) receptor antagonist than losartan. However, evaluating the antihypertensive efficacy of these drugs when administered systemically is complex due to several pharmacokinetic factors (e.g., metabolism and lipophilicity).

Angiotensin II↗
PubMedDate not supplied

Translation of salt retention to central activation of the sympathetic nervous system in hypertension.

1. Increased dietary salt increases blood pressure in many hypertensive individuals, producing salt-sensitive hypertension (SSH). The cause is unknown, but a major component appears to be activation of the sympathetic nervous system. The purpose of this short review is to present one hypothesis to explain how increased dietary salt increases sympathetic activity in SSH. 2. It is proposed that increased salt intake causes salt retention and raises plasma sodium chloride (NaCl) concentrations, which activate sodium/osmoreceptors to trigger sympathoexcitation. Moreover, we suggest that small and often undetectable increases in osmolality can drive significant sympathoexcitation, because the gain of the relationship between osmolality and increased sympathetic activity is enhanced. Multiple factors may contribute to this facilitation, including inappropriately elevated levels of angiotensin II or aldosterone, changes in gene expression or synaptic plasticity and increased sodium concentrations in cerebrospinal fluid. 3. Future studies are required to delineate the brain sites and mechanisms of action and interaction of osmolality and these amplification factors to elicit sustained sympathoexcitation in SSH.

Animals↗
PubMedDate not supplied

Thermoregulatory role of periventricular tissue surrounding the anteroventral third ventricle (AV3V) during acute heat stress in the rat.

1. Thermoregulatory effector mechanisms are strongly influenced by hydration status. Dehydration delays the onset of evaporative heat loss and the redistribution of cardiac output in response to elevations in core temperature, yet very little is known about how and where thermal and non-thermal information is integrated. 2. The anteroventral third ventricular (AV3V) region encompasses several distinct neural structures, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, the preoptic periventricular nucleus and the medial aspects of the medial preoptic nucleus. In addition to its well-documented role in body fluid and cardiovascular homeostasis, recent anatomical and in vitro evidence has indicated the AV3V region may also be pivotal in the integration of thermal and osmotic information. 3. Electrolytic lesions of the AV3V region produce a markedly reduced thermal tolerance in rats. Elevations in mean arterial pressure, heart rate and mesenteric resistance were all attenuated in the AV3V-lesioned animals in response to a heat stress; however, hindquarter resistance was unaffected. Heat-induced salivation was also attenuated, severely reducing the ability of rats to lose heat via evaporation. 4. The AV3V region clearly has a functional role in thermoregulation, as well as cardiovascular and body fluid homeostasis. These data add further support to the hypothesis that thermal and non-thermal information may be integrated within this region.

Acute Disease↗