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J Buggy

Publications and source records attributed to J Buggy.

At least 37 records · Page 2Linked to original sources
PubMed1984

3H-2-deoxyglucose uptake after electrical stimulation of cardioactive sites in anterior medial cortex in rabbits.

The anterior medial cortex is an important integrative area for cardiovascular adjustments occurring during learning and conditioning. The autoradiographic 3H-2-deoxyglucose (3H-2DG) method for regional cerebral metabolic activity was used to identify other forebrain regions associated with cardiovascular adjustments elicited by electrical stimulation of anterior medial cortex. Rabbits that received anterior midline stimulation that produced bradycardia and depressor responses showed increased metabolic activity in the ipsilateral mediodorsal (MD) nucleus of the thalamus and the dorsal aspect of the claustrum. Two additional animals with anterior cortical placements in the infralimbic and anterior limbic areas showed ipsilateral increased activity in perirhinal cortex, but more dorsolateral placements in the precentral agranular area did not produce increased perirhinal activity. Control animals did not show this pattern of activity. These data suggest that MD and claustrum participate in a neural circuit which mediates cardiovascular adjustments similar to those elicited by Pavlovian conditioning contingencies.

Animals↗
PubMed1984

Angiotensin-estrogen interaction in female brain reduces drinking and pressor responses.

Water intake fluctuates over the estrous cycle in rats, with daily intake lowest on the day of estrus. Since estrogen levels are highest preceding estrus and since the brain integrates thirst behavior, a possible central action of estrogen on fluid regulatory mechanisms was investigated in adult male and ovariectomized female rats. Ad libitum drinking was not changed the day of intracerebroventricular injection of estradiol benzoate (EB) but was significantly depressed the following day in females only. Drinking induced by intracerebroventricular angiotensin but not carbachol or cellular dehydration was also depressed in females the day after central EB treatment; again, no change occurred in males. To determine whether central EB depressed other centrally mediated responses to angiotensin, pressor responses to intracerebroventricular injections of angiotensin, carbachol, and hypertonic NaCl were also assessed. Only angiotensin-induced pressor responses in females were attenuated by central EB treatment, with a time course similar to that observed for the depression of drinking. We conclude that central regulatory responses to angiotensin are modulated by estrogen in female but not male brains.

Angiotensin II↗
PubMed1984

Periventricular forebrain mechanisms for blood pressure regulation.

Periventricular forebrain regions participate in body fluid and cardiovascular regulatory mechanisms that are intimately related to neural participation in experimental hypertension. Ablation of preoptic-hypothalamic periventricular tissue surrounding the anteroventral third ventricle (AV3V) disrupts both angiotensin (AngII) and sodium regulatory mechanisms and prevents experimental hypertension in either renin-dependent or -independent models. When AV3V is spared, and central AngII pressor mechanisms are interrupted by subfornical organ ablation or anterior hypothalamic knife cuts, renin-dependent but not renin-independent models of hypertension are prevented. Volume-expanded models of hypertension may be mediated by a natriuretic hormone that also inhibits the sodium-potassium pump in vascular smooth muscle, resulting in increased vasoconstriction. Volume expansion-induced release of this humoral ATPase inhibitor is attenuated in rats with AV3V lesions. In the renin-independent, reduced renal mass model, development of hypertension is correlated with increased plasma levels of sodium-potassium pump inhibitor. AV3V ablation blocks both the hypertension and the increase in humoral ATPase inhibitor. Thus, Thus, central angiotensin pressor and natriuretic mechanisms overlap in AV3V, and prevention of renin-dependent and volume-dependent models of experimental hypertension by AV3V ablation appears linked to disruption of these functionally separable systems.

Angiotensins↗
PubMed1983

Prevention of two-kidney, one-clip renal hypertension in rat by ablation of AV3V tissue.

This study examined the role of the anteroventral third ventricle (AV3V) in the renin-dependent two-kidney, one-clip model of renal hypertension. AV3V lesion and sham lesion rats were subjected to the placement of a clip on one renal artery or a sham operation. The sham lesion-renal artery clip rats experienced an increase in systolic blood pressure; however, AV3V lesioned animals experienced only a transient rise in arterial pressure during the 1st wk after clip. Body fluid regulation studies during the course of the hypertension revealed that there were no differences in water intake and urine volume between the lesion- and sham lesion-renal artery clip animals. Although significantly greater plasma and blood volumes were demonstrated in the AV3V lesion-sham clip rats compared with sham lesion animals, no differences in vascular volumes were detected in the renal artery clip rats. Finally, the rats were water deprived for 3 days to maximally stimulate vasopressin release. Urine osmolality increased significantly in all groups of rats except the AV3V lesion-renal artery clip animals protected against the hypertension.

Animals↗
PubMed1981

Prevention of renal hypertension and of the central pressor effect of angiotensin by ventromedial hypothalamic ablation.

Various lines of research have implicated the central nervous system in the development of renal hypertension. The ablation of a periventricular region surrounding the anteroventral third ventricle (AV3V) has been shown to block the development of renal hypertension. Because of hemodynamic effects produced by AV3V electrical stimulation can be abolished by a midline lesion of the ventromedial hypothalamic--median eminence region (VMH-ME), the effect of VMH-ME ablation on the development of renal hypertension was studied. Following recovery from surgery that destroyed the VMH-ME region the lesioned rats and controls were subjected to unilateral nephrectomy and figure-of-eight wrapping of the remaining kidney. Control animals developed renal hypertension but those with VMH-ME lesions did not. When the pressor response produced by intracerebroventricular injections of angiotensin II was studied, it was found that rats with VMH-ME lesions, as compared to neurologically intact animals, showed significantly attenuated responses. The data suggest that a neural system related to cardiovascular control descends through the VMH-ME region and that the integrity of this pathway is necessary for the development of renal hypertension.

Angiotensin II↗
PubMed1981

Brain functional activity during PAG stimulation-produced analgesia: a 2-DG study.

The autoradiographic 2-deoxyglucose method for regional cerebral metabolic activity was modified for use with tritium label to determine which brain stem and spinal cord nuclei changed their functional neural activity during periaqueductal gray stimulation-produced analgesia. The greatest changes in activity during electrical stimulation of the periaqueductal gray occurred in nucleus paragigantocellularis, the ventral portion of the nucleus reticularis gigantocellularis, and the nucleus cuneiformis. Substantial increases in metabolic activity were also evident in the spinal trigeminal nucleus and the substantia gelatinosa. Many of the regions which displayed increased functional activity in the present study have been shown to possess substantial enkephalin immunoreactivity. While several of these structures have previously been implicated in modulation of nociceptive transmission, this study raises the possibility that other brain stem nuclei may also participate in analgesic mechanisms.

Animals↗
PubMed1980

The area postrema plays no role in the pressor action of angiotensin in the rat.

The area postrema has been shown to have a major role in mediating the pressor effects of peripheral angiotensin in the dog, cat, and rabbit. The purpose of this study was to ascertain the function of the medullary circumventricular structure in the conscious rat. The pressor potency of angiotensin administered into the vertebral and carotid arteries was compared with intra-aortic infusions of angiotensin. Although no difference in pressor activity of angiotensin could be detected between intraaortic and intravertebral administration, greater sensitivity was observed during intracarotid infusion. No difference in the course of one-kidney renal hypertension was observed between sham-lesioned rats and animals with an area postrema lesion. In addition, lesioned and sham-lesioned animals showed equivalent responses to graded doses of angiotensin administered either intravenously or into the lateral ventricle. It was concluded that in the rat the area postrema plays no role in mediating the central nervous system actions of angiotensin whether the peptide reaches the brain via the blood or the cerebrospinal fluid.

Angiotensin II↗
PubMed1979

Role of central catecholamines in the control of blood pressure and drinking behavior.

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.

Animals↗
PubMed1979

Osmosensitivity of rat third ventricle and interactions with angiotensin.

Injections of hyperosmotic solutions (1- to 5-microliter injections of NaCl or sucrose solutions ranging in osmolarity from 0.34 to 0.90 osmol/l) into the anteroventral third ventricle (AV3V) of rats resulted in short latency drinking antidiuretic, and pressor responses. AV3V injections or infusions of combined angiotensin-hyperosmotic NaCl solution did not result in drinking greater than the sum of drinking to angiotensin and hyperosmotic NaCl separately administered. Differences in water versus saline drinking fluid preferences provided a behavioral dissociation of angiotensin and hyperosmotic sensitive neural mechanisms. Comparison of AV3V and lateral preoptic injection sites provided an additional separation since angiotensin was equally effective at both sites whereas osmotic stimulation was more effective at the AV3V site. AV3V lesions have previously been reported to abolish drinking, antidiuretic, and pressor responses to angiotensin and hyperosmotic stimulation. The data reported here provide additional evidence that angiotensin and hyperosmotic stimuli may both act on tissue surrounding AV3V but suggest that the neural substrates for these stimuli are not identical.

Angiotensin II↗
PubMed1978

Angiotensin-induced thirst: effects of third ventricle obstruction and periventricular ablation.

The role of periventricular tissue surrounding the anteroventral third ventricle (AV3V) in mediating drinking behavior induced by angiotensin II was investigated rats. Electrolytic lesions which bilaterally destroyed preoptic-hypothalamic periventricular tissue surrounding AV3V abolished drinking responses normally elicited by intracerebral injections of angiotensin. In another experiment, ventricular obstruction in AV3V had no effect on drinking of a palatable sweet milk solution while the drinking responses induced by peripheral versus central administration of angiotensin were dissociated. Drinking normally induced by lateral preoptic injections of angiotensin was no longer observed when AV3V obstruction prevented drug distribution via cerebrospinal fluid circulation to AV3V periventricular tissue; the drinking response induced by subcutaneous injection of angiotensin was enhanced, however, after placement of the ventricular obstruction. These results, coupled with the earlier observation that AV3V lesions also abolish drinking induced by subcutaneous angiotensin injectin, suggest that, after central or peripheral administration, angiotensin acts on AV3V periventricular tissue to arouse drinking. In contrast to centrally injected angiotensin, peripherally administered angiotensin does not contact receptors by entry and spread in cerebrospinal fluid. After peripheral injection angiotensin may contact sensitive AV3V tissue directly from blood, perhaps via the organum vasculosum of the lamina terminalis, a highly vascularized circumventricular organ within the AV3V which lacks a blood-brain barrier.

Angiotensin II↗
PubMed1978

Periventricular preoptic-hypothalamus is vital for thirst and normal water economy.

A midline stereotaxic lesion in rats destroying the periventricular tissue (lamina terminalis and preoptic-anterior hypothalamic periventricular stratum) surrounding the anteroventral third ventricle (AV3V) produces adipsia without other marked behavioral changes. Although food consumption is reduced in animals rendered adipsic by the lesion, feeding continued and intake is comparable to that of water-deprived-sham-lesioned animals. About half the rats recover drinking after a period of adipsia, but the others never resume water intake and become moribund. An analysis of urinary output indicates that adipsic animals fail to reduce urine volume and continue to elaborate an inappropriately dilute urine. The periventricular lesion-induced adipsia without compensating antidiuresis produces a significant rise in plasma protein, sodium, osmolality, and urea nitrogen which if untreated often results in acute encephalopathy leading to death. These data suggest that preoptic-anterior hypothalamic periventricular tissue houses vital neural elements which function in the modulation of water ingestive and conservation mechanisms directed at the maintenance of body fluid homeostasis.

Animals↗
PubMed1977

Preoptic-hypothalamic periventricular lesions: thirst deficits and hypernatremia.

To assess the significance of stimulation studies suggesting an anteroventral third ventricle (AV3V) dipsogenic site of action for hyperosmotic and angiotensin thirst stimuli, electrolytic lesions of periventricular tissue surrounding AV3V were produced under ether anesthesia in rats preselected for responsiveness to subcutaneous angiotensin and hypertonic NaCl thirst challenges. Lesions limited to preoptic-anterior hypothalamic periventricular substrates resulted in adipsia; those rats resuming ad lib. drinking after a period of adipsia exhibited persistent drinking deficits to angiotensin and hypertonic NaCl thirst challenges, reduced drinking after water deprivation, and increased plasma osmolality and sodium. Drinking to polyethylene glycol-induced hypovolemia and feeding after food deprivation did not differ between lesioned and sham-lesioned animals. The disturbances in behavioral control of fluid balance imply that AV3V periventricular tissue normally plays a key role in mediating regulatory drinking. It is proposed that these AV3V periventricular lesion-induced effects on drinking behavior are due to destruction of receptors and/or integrative systems monitoring fluid-borne angiotensin and hyperosmotic stimuli.

Angiotensin II↗
PubMed1977

Prevention of the development of renal hypertension by anteroventral third ventricular tissue lesions.

Several reports have suggested that a central action of the renin-angiotensin system plays a role in the development of renal hypertension. Based on the identification of the anteroventral thrid ventricle (AV3V) as a site of central angiotensin dipsogenic and pressor mechanisms, the present study examined the effect of electrolytic lesions in the AV3V region on the development of renal hypertension in rats. Lesioning alone produced a temporary but profound adipsia and, in one-half of the rats, a substantial transient elevation in arterial pressure. After lesioned rats had recovered normal drinking and blood pressure, unilateral nephrectomy with figure-of-eight wrapping of the remaining kidney failed to produce the hypertension and increased drinking observed after renal wrapping in shamlesioned rats. The possibility that the failure of lesioned rats to increase water intake after wrapping prevents hypertension development was ruled out by experiments demonstrating that normal rats exhibited identical rises in arterial pressure after wrapping regardless of whether or not they were allowed to increase water intake. The fact that unanesthetized lesioned rats exhibit attenuated drinking and pressor responses to systemically administered angiotensin suggests this mechanism as a possible explanation for the failure of AVV-lesioned rats to increase drinking and blood pressure after renal wrapping.

Angiotensin II↗
PubMed1976

Anteroventral third ventricle site of action for angiotensin induced thirst.

The central site of action for angiotensin induced thirst was investigated in rats. Subfornical organ lesions resulted in a temporary abolition of drinking induced by lateral preoptic or lateral ventricle microinjections of angiotensin but drinking to anteroventral third ventricle microinjections of angiotensin (or carbachol) was unaffected. Drinking to elevated systemic levels of angiotensin was attenuated but not abolished by subfornical organ lesions. When spread of injected angiotensin via cerebrospinal fluid circulation was controlled by placing plugs at selected locations in the ventricles, drinking was elicited only when intracranial microinjections of angiotensin gained access to anteroventral third ventricle. It was concluded that subfornical organ is not the exclusive dipsogenic receptor for angiotensin, rather angiotensin exerts at least part of its dipsogenic effect by spread through the ventricular system to receptors in the vicinity of the anteroventral third ventricle.

Angiotensin II↗
PubMed1975

Ventricular obstruction: effect on drinking induced by intracranial injection of angiotensin.

Lesions of the subfornical organ (SFO) severely attenuated drinking induced by injections of angiotensin II into the lateral ventricles, but a few days (4 to 14) later a recovery of the drinking response is observed. A possible explanation for this is that other dipsogenic sites are involved which are beyond the interventricular foramen and that SFO lesions produce an obstruction by edema or debris at the foramen which blocks access of cerebrospinal fluid-borne angiotensin to those sites. This hypothesis is supported by tracer studies and by direct injection into the third ventricle of SFO-lesioned animals. Other studies reported implicate the anteroventral third ventricle as a likely site for angiotensin receptors.

Angiotensin II↗