Search PubMed⌕ Search

Biomedical subjects

A K Johnson

Publications and source records attributed to A K Johnson.

At least 145 records · Page 8Linked to original sources
PubMed1990

Experimental dissociation of behavioral and cardiovascular outcome in the borderline hypertensive rat.

F1 Offspring of hypertensive and normotensive rats (BHR) were reared with either hypertensive (SHR) or normotensive (WKY) cagemates, and observations were conducted at two developmental periods to assess the effects of rearing condition on the social environment and the behavior of BHR subjects. SHR displayed significantly more agonistic behavior during development than WKY, and BHR subjects reared with SHR were the targets of significantly more agonistic behavior than BHR subjects reared with WKY cagemates. BHR reared with SHR initiated twice as much agonistic behavior as BHR reared with WKY. When heart rate and blood pressure were assessed at 75-80 days of age, however, neither the alterations in developmental social environment nor the alterations in the behavioral characteristics of BHR were associated with differences in cardiovascular variables. The results do not support a causal connection between behavioral characteristics and cardiovascular outcome.

Agonistic Behavior↗
PubMed1990

Role of beta 2-adrenoceptors in cardiovascular response of rats to acute stressors.

The role of peripheral beta 2-adrenoceptors in the cardiovascular response to acute stress was examined in adult Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and the first generation (F1) cross of WKY and SHR. In experiment 1, WKY, SHR, and F1 were exposed to two stressors, transfer to a novel chamber and foot shock, after treatment with either vehicle or the beta 2-adrenoceptor antagonist ICI 118,551. SHR and F1 treated with ICI 118,551 had greater pressor responses to the stress of transfer and to foot shock than vehicle-treated controls. In contrast, the cardiovascular response of WKY to the stressors was not affected by beta 2-adrenoceptor antagonism. These results suggest that beta 2-adrenoceptors are activated during acute stress in SHR and F1 to reduce large pressor episodes, but this mechanism is not utilized in WKY. A second study examined the effects of beta 2-adrenoceptor antagonism on resting arterial pressure. Resting heart rate and pressure were not significantly different between vehicle- and ICI 118,551-treated animals. However, the pressor response to the stressors was greater in ICI 118,551- than vehicle-treated F1, but the tachycardia was equivalent for both groups. These results demonstrate that beta 2-adrenoceptor antagonism can selectively enhance pressor responses to stress without affecting heart rate responses. Together, these results suggest that activation of beta 2-adrenoceptors during acute stress may blunt large pressor responses in SHR and F1, which may be related to the exaggerated sympathoadrenal response to stress that is characteristic of SHR.

Acute Disease↗
PubMed1990

Area postrema and differential reflex effects of vasopressin and phenylephrine in rats.

In normal rats, baroreflex inhibitions of heart rate (HR) and splanchnic but not lumbar sympathetic neural activity (SNA) are greater when mean arterial pressure (MAP) is increased by intravenous infusion of arginine vasopressin (AVP) compared with phenylephrine (PE) or methoxamine. In normal rabbits, baroreflex inhibitions of HR and lumbar and renal SNA are all greater when MAP is increased by AVP vs. PE. The differential reflex bradycardic and renal sympathoinhibitory effects of AVP vs. PE in rabbits require an intact area postrema. To determine whether differential reflex effects of AVP vs. PE in rats is selective for HR or inclusive of renal SNA and to examine the role of the rat area postrema in such action, we monitored HR and renal SNA in normal (sham operated, n = 8) and area postrema-lesioned (APX, n = 8) rats under chloralose anesthesia during slow increases in MAP (less than 0.3 mmHg/s; 3 min) induced intravenously by AVP (0-16 mU.kg-1.min-1) and by PE (0-8 micrograms.kg-1.min-1). Reflex inhibition of HR (-delta betas.min-1.delta mmHg-1) was greater when MAP was increased by AVP vs. PE in normal rats (-2.7 +/- 0.5 vs. -1.7 +/- 0.1, P less than 0.05), and this difference was absent in APX rats (-2.5 +/- 0.5 vs. +/- -2.2 +/- 0.4). Similarly, maximum bradycardia (-delta beats/min) by AVP vs. PE was greater in normal rats (-64 +/- 8 vs. -48 +/- 7, P less than 0.05) but not in APX rats (-53 +/- 5 vs. -52 +/- 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Light-dark cycle modulates drinking to homeostatic challenges.

Both homeostatic and rhythmic variables are empirically and theoretically important controls of behavior. Yet, drinking behavior has been studied largely from one point of view or the other. The present study examined both homeostatic and rhythmic variables and found evidence for an important interaction of these two types of control of drinking behavior. The drinking rhythm of rats on a light-dark cycle was established. Water intake after cellular- or extracellular-related challenges was then measured both at a time of a peak and at a time of a trough of the drinking rhythm. The results indicate that rats drink more water after challenges in their early active phase than in their early inactive phase. The results demonstrate that rhythmic variables modulate the homeostatic controls of drinking behavior. The importance of the interaction of homeostatic and rhythmic variables in models of integrative control of behavior is discussed.

Adolescent↗
PubMed1990

Efferent mechanisms mediating renal sodium and water excretion induced by centrally administered serotonin.

Treatments that increase central extracellular serotonin (5-HT) also increase Na excretion. Efferent renal sympathetic nerve activity (ERSNA) contributes to the control of Na and water reabsorption. To determine whether renal nerves play a role in the 5-HT-induced natriuresis, we examined the effect of intracerebroventricular (icv) injection of vehicle or 5-HT (20 micrograms) on Na, K, and urine excretion rates, as well as mean arterial pressure and heart rate in unanesthetized, hydrated rats with renal nerves intact or sectioned. Renal denervation attenuated the natriuresis produced by 5-HT but not the antidiuresis observed 15-30 min after injection. Central 5-HT produced brief pressor and bradycardic responses, followed by continued bradycardia and hypotension, which were more pronounced in intact rats. In other experiments, circulating levels of arginine vasopressin (AVP) and plasma atrial natriuretic polypeptide (ANP) were measured 15 min after icv injection of 5-HT. 5-HT significantly increased circulating AVP, but plasma ANP remained unchanged. These results suggest that renal nerves participate in the natriuresis elicited by centrally administered 5-HT through a decrease in ERSNA. The antidiuresis observed after central 5-HT may be due to an increase in AVP release.

Animals↗
PubMed1990

Effects of sympathetic activation on plasma renin activity in the developing rat.

The present experiments studied the ontogeny of sympathetic control of the renin-angiotensin system by using pharmacological agents, which act at different levels of the sympathetic axis, to increase plasma renin activity (PRA) during the preweanling period in Sprague-Dawley rats. The selective beta-1 adrenoceptor agonist, prenalterol, produced age- and dose-dependent PRA increases. In 5- and 10-day-old animals, prenalterol treatment produced minimal stimulation of PRA and the dose-response curve was essentially flat. In contrast, greater PRA responses to increasing doses of prenalterol were found in 15- and 20-day-old animals. The PRA response to tyramine, which causes norepinephrine release from postganglionic sympathetic fibers, gradually increased between 5 and 20 postnatal days of age, first producing significant stimulation on day 15. Centrally mediated sympathetic activation with yohimbine also produced age-dependent stimulation of PRA that was comparable to the increases produced by tyramine between postnatal days 10 and 20. However, in contrast to tyramine, yohimbine produced a significant increase in PRA on postnatal day 5. The present results suggest that functional sympathetic control of the renin-angiotensin system matures during the second to third postnatal week in the Sprague-Dawley rat, and this may be related to the development of beta-1 adrenoceptors in the kidney that regulate renin release.

Age Factors↗
PubMed1989

Neuropeptide Y-immunoreactive cells in the caudal medulla project to the median preoptic nucleus.

The region surrounding the anteroventral third ventricle, particularly the median preoptic nucleus, has been implicated in the control of fluid balance and blood pressure. Previous studies indicate that catecholaminergic inputs from the caudal medulla are important in these controls. In this study we report that neuropeptide Y-immunoreactive cells in the caudal medulla project to the median preoptic nucleus in the basal forebrain. Notably these cells are found in the caudal ventral lateral medulla and the nucleus of the solitary tract. Since catecholaminergic projections to the median preoptic nucleus also arise from these regions the possibility of interactions between NPY and catecholamines exists, particularly in the control of fluid balance and blood pressure.

Animals↗
PubMed1989

Activation of supraoptic magnocellular neurons by gamma 2-melanocyte stimulating hormone (gamma 2-MSH).

The effects of intracarotid infusions of the peptide gamma 2-melanocyte stimulating hormone (gamma 2-MSH) on electrophysiologically and immunohistochemically identified supraoptic nucleus (SON) units were investigated. Over a wide dose range this agent always excited SON units, while control infusions of vehicle had no effect. Because neural responses invariably preceded blood pressure elevation, it appears that gamma 2-MSH excitation of the magnocellular system was due to a direct effect on the central nervous system and was not a result of systemic cardiovascular responses. These results suggest a forebrain gamma 2-MSH sensitive site in the activation of SON magnocellular neurons.

Action Potentials↗
PubMed1989

Decreased norepinephrine in the ventral lamina terminalis region is associated with angiotensin II drinking response deficits following local 6-hydroxydopamine injections.

Previous studies have demonstrated that punctate injections of 6-hydroxydopamine (6-OHDA) into structures along the ventral lamina terminalis reduce drinking responses elicited by angiotensin II (ANG II). The purpose of the present study was to extend these findings by quantifying the catecholamine depletions that are associated with the drinking response deficits. Male Sprague-Dawley rats were given injections of 6-OHDA into the median preoptic nucleus (MnPO) and the organum vasculosum of the lamina terminalis (OVLT) after pretreatment with pargyline. Controls were injected with vehicle and a third group received 6-OHDA after pretreatment with desmethylimipramine (DMI). All subjects were tested for drinking responses to centrally injected ANG II and carbachol. Changes in catecholamine content of the MnPO, OVLT, supraoptic nucleus, paraventricular nucleus, caudate and cortex were determined using HPLC with electrochemical detection after behavioral testing. Only rats injected with 6-OHDA without DMI pretreatment showed a significant reduction in ANG II-induced drinking responses. This behavioral deficit was associated with a significant norepinephrine decrease in the ventral lamina terminalis region. All 3 groups showed comparable drinking responses to carbachol. These data support the hypothesis that noradrenergic innervation of the ventral lamina terminalis region is necessary for ANG II-induced drinking responses.

Angiotensin II↗
PubMed1989

Effects of behavior and social condition on cardiovascular response to footshock stress.

Rats were instrumented with arterial catheters and directional-pulsed Doppler flow probes for assessment of blood pressure, heart rate, and blood flow in the renal, mesenteric, and hindquarter vascular beds. Subjects were tested in an intermittent shock procedure under paired and isolated social conditions and the cardiovascular indices associated with first shock, prone immobile behavior, upright behavior, and boxing behavior were recorded. Both shock procedures resulted in increased heart rate, mesenteric resistance, and renal resistance, as well as decreased hindquarter resistance. Blood pressure response was variable. Social and behavioral conditions generally accounted for little variance in cardiovascular indices during the treatments. Blood pressure assessed 2.5 min after the last shock was significantly higher in the isolated shock condition. In the context of divergent results from previous research in the area, the current results are most consistent with the view that a similar form of cardiovascular adjustment is present under paired and isolated shock, but that under some conditions the presence of a conspecific or the opportunity to fight may attenuate cardiovascular response to shock.

Aggression↗
PubMed1989

Cardiovascular and sympathetic nervous system responses to an acute stressor in borderline hypertensive rats (BHR).

The present study examined cardiovascular and plasma catecholamine responses to acute footshock stress in adult male Wistar-Kyoto (WKY) normotensive, borderline hypertensive (BHR), and spontaneously hypertensive (SHR) rats. Basal mean arterial pressure and heart rate were equivalent for SHRs and BHRs, and levels for both groups were elevated compared to WKYs. Following transfer to the footshock chamber, blood pressure increased to a greater degree in SHRs than in WKYs or BHRs. However, the tachycardia was exaggerated in both BHRs and SHRs compared to WKYs. In response to intermittent footshock stress, all groups had comparable heart rate increases while maintaining blood pressure near baseline levels. SHRs demonstrated a sympathetic hyperresponsiveness to footshock stress, with greater increases in plasma norepinephrine and epinephrine levels than WKYs immediately following footshock. At 5 minutes postfootshock, plasma catecholamines remained elevated in SHRs over both WKYs and BHRs. Plasma catecholamine increases following footshock were comparable at all time points between WKYs and BHRs. The present results demonstrate that sympathetic responsiveness of BHRs to acute footshock stress is more similar to normotensive WKYs than to hypertensive SHRs.

Animals↗
PubMed1989

The supraoptic nucleus: afferents from areas involved in control of body fluid homeostasis.

Physiological evidence indicates that the supraoptic nucleus may be an important integrating region for information relating to body fluid homeostasis. It is known that the supraoptic nucleus receives neural influences from brain receptive zones for plasma osmolality and angiotensin II, as well as from relay centers for blood pressure and blood volume. It is also known that these influences interact to modulate vasopressin release from the supraoptic nucleus. Therefore, a detailed investigation of the neurochemical afferents to the supraoptic nucleus from regions of the lamina terminalis and the brainstem was undertaken. Injection of a fluorescent retrograde tracer, doxorubicin, into the supraoptic nucleus was combined with histochemistry of angiotensin II and catecholamines. Following supraoptic nucleus injection, retrograde label was found in forebrain neurons of the subfornical organ, median preoptic nucleus, and organum vasculosum of the lamina terminals. Some labeled cells in the subfornical organ and organum vasculosum of the lamina terminalis were also found to contain angiotensin II immunoreactivity. In the brainstem, retrograde label was found in neurons of the A1, A2 and A6 cell groups. Many of these cells were also found to contain catecholamine fluorescence or tyrosine hydroxylase immunoreactivity. Corroboration of the A2 projection was obtained by lesions of this nucleus, which reduced catecholamine fluorescence in the supraoptic nucleus. These findings provide an anatomical basis for the functional observations that the supraoptic nucleus plays a key integrative role in the maintenance of body fluid homeostasis.

Angiotensin II↗
PubMed1989

Haemodynamic responses to conflict stress in borderline hypertensive rats.

Chronic exposure to a shock-shock conflict paradigm (2 h/day, 5 days/week for 12 weeks [1]) produces hypertension in the borderline hypertensive rat (BHR), a cross between the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto rat (WKY). The purpose of the present study was to characterize the regional haemodynamic responses which take place during conflict-stress. A pulsed Doppler flowmeter and miniature probes implanted on the left renal and superior mesenteric arteries and the abdominal aorta were used to record changes in regional flow velocity. Recording of mean arterial pressure (MAP) allowed changes in regional resistance to be calculated. The first conflict session produced intense splanchnic and renal vasoconstriction and hindquarter vasodilation. Pressor responses were moderate. A second group of BHRs was studied during conflict sessions 17-18, prior to the development of hypertension. This group exhibited faster habituation to the stress than the group studied during the first conflict session: MAP and mesenteric resistance returned more rapidly towards pre-stress levels. Relative to naive control rats, this group exhibited a larger peak MAP and less tachycardia in response to a neutral stressor (air-jet stress) and a smaller reduction in renal resistance in response to ganglionic blockade. These data suggest that in this model, pressure load per se is moderate. More attention should be directed towards the role of trophic effects of the neurohumoral factors responsible for the pronounced constriction of splanchnic and renal vasculature in producing hypertension.

Analysis of Variance↗
PubMed1989

Central oxytocin systems may mediate a cardiovascular response to acute stress in rats.

The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.

Acute Disease↗
PubMed1989

Brain stem mechanisms and the inhibition of angiotensin-induced drinking.

The present studies examine the effect of lesions of the ventrolateral region of the lateral parabrachial nucleus (VLLPBN) and of the area postrema and medial region of the nucleus of the solitary tract (AP/mNTS) on water intake induced by intracerebroventricular administration of angiotensin II (ANG II) and of the cholinergic receptor agonist, carbachol. Water intake was measured in rats with bilateral electrolytic lesions of the VLLPBN or thermocautery ablation of the AP/mNTS after intracerebroventricular delivery of ANG II (50 and 100 ng/2 microliter), carbachol (100 and 250 ng/2 microliter), and isotonic saline (2 microliter). Rats with lesions of the VLLPBN drank significantly more water during a 30-min test period to both doses of ANG II, but not to carbachol, than did sham lesion rats. Similarly, AP/mNTS lesion rats drank significantly more than sham lesion animals in response to the high dose of ANG II but not to carbachol. These results suggest that the previously reported exaggerated drinking responses to systemically administered ANG II demonstrated by rats with either VLLPBN or AP/mNTS lesions is not the result of a direct peripheral action of the octapeptide. Furthermore, the similarity of the induced drinking responses produced by these two lesions suggests that the AP/mNTS and the VLLPBN may be linked in a common thirst-mediating pathway.

Angiotensin II↗
PubMed1989

Lesions of the anteroventral third ventricle and development of stress-induce hypertension in the borderline hypertensive rat.

The anteroventral third ventricle (AV3V) region plays a critical role in the pathogenesis of many forms of experimental hypertension. The present study sought to determine whether the integrity of this area was necessary for the development of stress-induced hypertension in the borderline hypertensive rat (BHR). Male BHRs were assigned to three groups at 8 weeks of age: 1) AV3V lesion, 2) sham lesion, and 3) maturation control. BHRs with AV3V and sham lesions were exposed to 12 weeks of conflict stress (2 hr/day, 5 days/wk). At the end of the conflict protocol period, direct measurement of resting mean arterial pressure indicated that BHRs with sham lesions had significantly higher blood pressure (153 +/- 2.9 mm Hg) than rats with AV3V lesions (126 +/- 5.2 mm Hg) and maturation control rats (133 +/- 4.3 mm Hg). Although AV3V lesions prevented stress-induced hypertension in BHRs, these rats were still capable of transiently raising blood pressure. Specifically, the results also indicate that BHRs with AV3V lesions showed greater increase in blood pressure in response to an electric foot-shock paradigm. This study suggests a critical role for this forebrain region in the production of stress-induced hypertension in genetically predisposed animals.

Animals↗
PubMed1989

Lesions of the anteroventral third ventricle prevent salt-induced hypertension in the borderline hypertensive rat.

Many forms of experimental hypertension depend on the integrity of the periventricular tissue surrounding the anteroventral third ventricle. The current investigation examined the extent to which this forebrain area is necessary for the elaboration of salt-induced hypertension in the borderline hypertensive rat. Eight-week-old male rats were given either electrolytic lesions of the anteroventral portion of the third ventricle region or sham lesions. All rats were then placed on a high salt diet (8% NaCl) for 10 weeks. At the conclusion of this dietary period, direct measurement of resting mean arterial pressure revealed that borderline hypertensive rats with lesions of the anteroventral portion of the third ventricle had significantly lower blood pressure (128.4 +/- 5.1 mm Hg) compared with sham-operated rats (148.1 +/- 4.1 mm Hg).

Analysis of Variance↗