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Biomedical subjects

M I Phillips

Publications and source records attributed to M I Phillips.

At least 199 records · Page 11Linked to original sources
PubMed1976

Regional study of cerebral ventricle sensitive sites to angiotensin II.

Angiotensin II injected in small doses into the cerebral ventricles produces an increase in blood pressure and drinking behavior. The site of action for both of these effects was studied in 3 main experiments. (1) The response to several doses of angiotensin delivered to each ventricle was investigated with multiple ventricular cannulation. This revealed that the rostral ventricular system was involved in angiotensin II mediated responses. (2) CSF flow was limited by plugging specific anterior and posterior ventricular regions and then testing for angiotensin II induced drinking and pressor responses. This technique showed that the ventral anterior third ventricle must be reached by the peptide in order to produce either blood pressure or drinking effects. (3) In order to separate pressor components due to vasopressin release and sympathetic activation, hypophysectomized rats were also tested. The experiment showed that the pressor response to intraventricular angiotensin II is due to both sympathetic and pituitary hormonal components and both are dependent on sites sensitive to angiotensin in the anterior third ventricule. The ventral anterior third ventricle or periventricular tissue surrounding it seems to be essential for both blood pressure and drinking responses to intraventricular angiotensin II.

Angiotensin II↗
PubMed1976

Specific angiotensin II receptive neurons in the cat subfornical organ.

To test if neurons in the subfornical organ (SFO) are specifically sensitive to angiotensin II (AII) we have applied the AII analog sar1-ala8-AII (P113) directly on to cells in the SFO by microiontophoresis. Adult cats were anesthetized and the SFO exposed for penetration by a 5-barreled micropipette electrode. Of 22 units which responded positively to AII, 7 were also positive to acetylcholine. P113 alone produced either no effect or a decrease in unit firing. P113 plus AII produced antagonism in 17 of 18 units. P113 plus acetylcholine produced antagonistic effects in 5 of 14 cases. Only two units were completely antagonized and 5 units showed agonistic interaction. The most sensitive antagonism with respect to dose of P113 was on neurons responsive only to AII and not to both AII and acetylcholine. We conclude that there are specific AII neurons in the SFO.

Acetylcholine↗
PubMed1976

Evidence for sar1-ala8-angiotensin crossing the blood cerebrospinal fluid barrier to antagonize central effects of angiotensin II.

Injections of angiotensin II into the cerebral ventricles of the rat produces both a drinking and a pressor response. We have measured both responses simultaneously in conscious animals. The effect of saralasin acetate (P113), a specific angiotensin II competitive antagonist, has been studied on these angiotensin II induced responses. The results show that: (1) P113 given intravenously (i.v.) in doses of 500 ng/min or 1800 ng/min has no observable effect on 50 ng angiotensin given intraventricularly (IVT). At 72 mug/min, however, there was a 55% reduction in the drinking and pressor responses to 50 ng angiotensin II (IVT); (2) 500 ng of P113 given IVT abolished the effects of 50 ng angiotensin II also given IVT and (3) P113 given i.v. at all doses antagonized the pressor effects of angiotensin II (i.v.) responses. The data indicate that both the drinking and pressor responses to angiotensin II (IVT) injections are centrally mediated and show that when a high enough dose of P113 is given peripherally the central effects of angiotensin II can be reduced. This suggests that a fraction of the P113 injected i.v. may pass across the blood-CSF barrier. Since P113 has a similar structure to angiotensin II the results have implications for studies in which high peripheral doses of angiotensin II are used.

Angiotensin II↗
PubMed1976

The effect of subfornical organ lesions and ventricular blockade on drinking induced by angiotensin II.

The role of the subfornical organ (SFO) as the unique receptor site for the drinking behavior induced by intracranial injections of angiotensin II (AII) was investigated. It was found that: (1) drinking in response to intraventricular (IVT) injections of AII was reduced in 6 rats but was unchanged after 80-100% damage of the SFO in 4 cases; (2) reduction of drinking to lateral ventricular application of AII was seen with no apparent SFO damage in 4 rats; (3) recovery of the AII induced drinking deficit was consistently observed within a short time interval (14 days), even in those animals with complete SFO lesions: (4) the presence of ventricular debris was correlated with deficits in water intake to IVT angiotensin injections. In a second experiment artificial blockade of the ventricular space was produced by a plugging technique. Plugging the anterior third ventricle simulated the effects of SFO lesioning. It was concluded that the SFO is not a unique receptor area since the ventral anterior third ventricle is also sensitive for AII (IVT) induced drinking. If the SFO is a receptor site for AII circulating in the CSF it is probably not the only periventricular receptor site. Access of AII to the anterior ventral third ventricle appears to be essential for inducement of drinking.

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↗
PubMed1969

Unit activity: motiviation-dependent responses from midbrain neurons.

Single neurons in the midbrain tegmentum of rats showed clear discriminatory responses to three tones announcing either food or water or no reinforcement. Subjects were required to press a single lever and remain motionless for 2 seconds during which time unit activity from several brain sites was recorded. One of the tones, randomly designated, was sounded halfway through this period. Manipulation of drive states revealed that the highest activity was associated with tones announcing the reinforcement for which the animal was most strongly motivated. Thus, from a hungry animal sustained or increased firing rates were elicited by a " food" tone and differentially lowered rates by the other tones.

Animals↗
PubMedDate not supplied

Influence of EGTA on an exercise-induced elevation in the colonic temperature of the rat.

The purpose of this study was to determine if an exercise-induced rise in body temperature could be affected by the chelation of Ca++ in the extracellular fluid surrounding the hypothalamus of the rat. Following the implantation of a guide tube above the hypothalamus, each animal was familiarized with exercising on a motor-driven treadmill. In random order, on separate days, a solution containing 3.6 mM EGTA, 26 mM Ca++ or an artificial cerebrospinal fluid (ACSF) solution was perfused through the guide tube while the animal was running. Colonic (Tc) and tail-skin (Tt) temperatures were monitored continuously. The perfusion of EGTA produced a significant increase in Tc when compared with the perfusion of the ACSF solution. The perfusion of excess Ca++ produced a significant decrease in Tc. These results suggest that Ca++ may play an important role in the mediation of heat dissipation during exercise.

Animals↗