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Biomedical subjects

J Kucharczyk

Publications and source records attributed to J Kucharczyk.

At least 91 records · Page 5Linked to original sources
PubMed1978

Drinking and haemodynamic changes induced in the dog by intracranial injection of components of the renin-angiotensin system.

1. Intracranial injections of the individual components of the renin-angiotensin system caused drinking in water-replete dogs. 2. Angiotensin II was the most reliable, potent and rapidly acting intracranial dipsogen and elicited drinking in the absence of peripheral circulatory changes. After the highest dose of angiotensin II (10(-9) mole) five dogs drank a mean amount of 380.0 +/- 88.6 ml. For the other components, the order of dipsogenic effectiveness was angiotensin I, synthetic renin substrate, and angiotensin III. 3. Isotonic saline, bradykinin (10(-10) mole), eledosin-hexapeptide (10(-10) mole), oxytocin (10(-10) mole) and prostaglandin F2alpha (1-200 X 10(-12) mole) were ineffective. 4. Intracranial renin (10 m-u.) produced a mean intake of 445 +/- 152 ml. of water in eight dogs. 5. Dog renin substrate and synthetic renin substrate, injected intracranially in a dose of 10(-10) mole, produced similar intakes of water but these amounts were very much less than the volume drunk in response to the same dose of angiotensin II. 6. None of the components injected into dipsogenically responsive sites in the brain caused changes in blood pressure, although the act of drinking itself produced a small rise. 7. Angiotensin II at the highest dose produced drinking when injected into the subfornical organ, preoptic region, anterior hypothalamus, lateral ventricle, third ventricle, ventral hippocampus and mid-line thalamus. Negative sites were found in the caudate nucleus, fourth ventricle, mid-brain, posterior thalamus, dorsal hippocampus, lateral hypothalamus and posterior hypothalamus. 8. After the lowest dose of intracranial angiotensin II (10(-12) mole) only the preoptic region and subfornical orgal were responsive. These two sites were equally sensitive in terms of latency and amounts drunk at all doses injected. 9. Angiotensin did not necessarily have to reach a cerebral ventricle in order to cause drinking. 10. The dog resembles the rat in its responsiveness to the dipsogenic action of intracranial angiotensin II. The regions of the brain from which drinking can be elicited are more widespread than has been claimed by some in the rat.

Angiotensinogen↗
PubMed1978

Systemic angiotensin-induced drinking in the dog: a physiological phenomenon.

1. Intravenous infusion of the individual components of the renin-angiotensin system caused drinking in dogs in water balance. 2. Angiotensin II was the most potent and rapidly acting peptide inducing drinking. The minimum effective rate of infusion was between 8.3 and 16.6 X 10(-12) mole kg-1 min-1 which yield blood levels of angiotensin II that fell well within physiological limits for the dog and were mildly pressor. Angiotensin I and synthetic renin substrate caused less drinking than angiotensin II, and angiotensin III was the least effective dipsogen. 3. Renin caused significant drinking when infused I.V. at a rate of 0.5 u. min-1 for 15 min. Drinking was slower in onset and continued for longer than after other components of the renin-angiotensin system. 4. Within the dose range 1875-15,000 X 10(-12) mole of angiotensin II the amount of water drunk depended more on the rate of infusion than on the duration of the infusion. 5. During an I.V. infusion of angiotensin II lasting 2 hr, the rate of drinking was greatest during the first 15 min. After this declined progressively. 6. A delay of 1 hr after the start of an intravenous infusion of angiotensin II before access to water was allowed, did not significantly reduce the amount of water drunk. Nor did infusion of isotonic saline for 105 min reduce drinking in response to a subsequent infusion of angiotensin II. However, a preload of dilute milk approximately equal in volume to the amount of water normally drunk in response to I.V. angiotensin II significantly reduced drinking. Therefore the dog stopped drinking during long-term infusions of angiotensin II owing to the action of satiety mechanisms and not to tachyphylaxis or fatigue. 7. Intracarotid infusion of angiotensin II, angiotensin I, synthetic renin substrate and angiotensin III, at 40 X 10(-12) mole min-1 also caused drinking. Intakes of water were similar to the intakes after I.V. infusion at six times the arterial rate, except that angiotensin I was relatively less effective by intracarotid infusion than by I.V. infusion. 8. Renin, infused at 0.5 u. min-1 for 15 min, was much less effective by intracarotid infusion than by intravenous. 9. These results are compatible with a role for circulating angiotensin II in the thirst of hypovolaemia or moderate extracellular dehydration.

Angiotensin II↗
PubMed1978

Central neural pathways for angiotensin-induced thirst.

Evidence is reviewed implicating the preoptic region in angiotensin-induced thirst. The most responsive area according to results obtained with behavioral, electrophysiological, and autoradiographic mapping techniques is at the caudal border of the medial preoptic region and rostral border of the anterior hypothalamus. The neural pathway from this preoptic site for angiotensin-induced thirst extends along the medial forebrain bundle through the midlateral hypothalamus to the paramedial midbrain tegmentum and to an area ventrolateral to the central gray. Lesions of this pathway in the midlateral hypothalamus and rostral midbrain significantly attenuated drinking induced by microinjections of angiotensin II into the preoptic area but did not disrupt water intake induced by microinjections of angiotensin II into the subfornical organ or cerebral ventricles. Although the efferent pathways from angiotensin-receptive sites in the subfornical organ and cerebral ventricles are unknown, it appears from these observations that the medial forebrain bundle is not involved. Lesions of the medial forebrain bundle-lateral hypothalamus also do not disrupt drinking induced by microinjections of hypertonic saline into the preoptic region although lesions placed 1 mm further lateral do. Since fat lateral hypothalamic lesions are without effect on drinking induced by centrally administered angiotensin II, this suggests that intracellular and extracellular thirst signals are subserved by separate neural pathways in the hypothalamus.

Action Potentials↗
PubMed1977

The role of mesencephalic structures in thirst induced by centrally administered angiotensin II.

(1) In 27 animals microinjection of 25--100 ng of angiotensin II through chronic cannulae implanted in the preoptic region initiated drinking and in subsequent acute experiments influenced the spontaneous discharge rate of single neurons in the ipsi-lateral mesencephalon. Of 148 neurons for which recordings were made, 52 (35%) increased their frequency of spike potentials following administration of angiotensin II, 2 (1%) showed inhibition and 94 (64%) showed no change in firing rate. (2) In another series of 44 animals, unilateral or bilateral lesions of the midbrain ventral tegmentum or reticular formation were found to have little or no effect on water intake elicited by the microinjection of angiotensin II into the preoptic region. (3) In contrast to the effects of tegmental and reticular lesions, unilateral lesions located dorsally and laterally to the mammillary peduncle, in the area of passage of the medial forebrain bundle, significantly attenuated the dipsogenic response to either contralateral or ipsilateral injections of angiotensin II into the preoptic region. With bilateral lesions this effect was permanent. (4) Since the more caudal lesions were relatively ineffective in disrupting the elicited drinking, it is suggested that signals from angiotensin II receptors in the preoptic region are transmitted along pathways which diverge in the midbrain. (5) The possibility of a forebrain-hypothalamus-midbrain circuit mediating thirst initiated by activation of the renin-angiotensin system is discussed.

Action Potentials↗
PubMed1977

Effect of preoptic administration of angiotensin on lateral hypothalamic unit activity.

The effect of administering angiotensin II to the preoptic region on lateral hypothalamic single unit activity was studied in unanesthetized, freely-moving rats. Angiotensin (100 ng) reliably initiated drinking behavior and caused an increase in the discharge frequency of single neurons located in the perifornical area but had no effect on units in the zona incerta, ventromedial hypothalamus or farlateral hypothalamus. These results suggest that efferent pathways from preoptic receptors for angiotensin pass through the midlateral hypothalamus.

Action Potentials↗
PubMed1977

Self-stimulation of the subfornical organ and lateral hypothalamus: differential effects of atropine and methysergide.

The effects of cholinergic blockade of neurons by atropine or serotonergic blockade by methysergide was investigated in rats responding for brain-stimulation reward. Bipolar stimulating electrodes were placed either in the subfornical organ (SFO) or the lateral hypothalamus (LH). Atropine sulphate and methysergide significantly suppressed self-stimulation of the SFO but not of the LH, suggesting that cholinergic and serotonergic neurons are involved in brain-stimulation reward associated with this site.

Amphetamine↗
PubMed1976

Differential effects of brain lesions on thirst induced by the administration of angiotensin-II to the preoptic region, subfornical organ and anterior third ventricle.

(1) The possibility that water intake elicited by the administration of angiotensin-II to the preoptic region (POA), subfornical organ and anterior third ventricle is mediated by separate neural systems was investigated in 58 male Wistar rats using electrolytic lesion techniques. (2) Lesions of the midlateral hypothalamus and paramedial rostral midbrain produced a significant reduction in water intake to angiotensin-II microinjected into the POA but did not affect drinking following administration of angiotensin-II to the subfornical organ or anterior third ventricle. (3) Ablation of the midlateral hypothalamus, paramedial rostral midbrain, habenular nucleus or interpeduncular nucleus had no significant effect on water intake elicited in response to microinjection of carbachol or hypertonic saline into the preoptic region, subfornical organ or anterior third ventricle. (4) In a second series of 12 animals lesions of the subfornical organ attenuated water intake in response to a peripheral injection of renin or isoproteronol without disrupting drinking to peripheral administration of hypertonic saline or polyethylene glycol or to 24 h water deprivation. (5) It is concluded that separate neural systems mediate water intake elicited by administration of angiotensin-II to the preoptic area, subfornical organ and anterior third ventricle. The possible physiological significance of independent and parallel peripheral and cerebral renin-angiotensin systems for the control of drinking behavior mediated by angiotensin-II is discussed. (6) The present results are in agreement with previous work which indicates that water intake induced by central administration of angiotensin-II, carbachol and hypertonic saline is subserved by different neural substrates.

Angiotensin II↗
PubMed1975

Separate lateral hypothalamic pathways for extracellular and intracellular thirst.

Small lesions of the midlateral zone of the lateral hypothalamus in rats attentuated water intake elicted by the central microinjection angiotensin or by the peripheral injection of isoproterenol or renin without attenuating drinking to peripherally administered hypertonic saline. Lesions placed further lateral in the hypothalamus, which destroyed the medial aspects of the internal capsule and globus pallidus, produced a marked decrease in water intake induced by hypertonic saline. Abaltion of the ventromedial nucleus of the hypothalamus increased drinking elicited by angiotension, isoproterenol, or renin. These results suggest that extracellular and intracellular thirst stimuli are mediated by separate neural pathways at the level of the lateral hypothalamus.

Angiotensin II↗