Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II, if injected into the lateral ventricles of rabbits in doses of 0.015-0.15 microgram, has an inhibitory action on the fear response evoked by electrical stimulation of the ventromedial hypothalamic nucleus, but in doses of 1-10 ng it blocks the inborn behavioral fear responses in rats. On microionophoretic application of angiotensin II to single neurons in the cerebral cortex and parafascicular complex of the thalamus, predominantly activation responses were observed. Predominance of inhibitory neuronal responses were noted in structures of the hypothalamus and mesencephalic reticular formation to angiotensin II. Responses of cortical and subcortical neurons to angiotensin II are potentiated after stimulation of the "fear center" in the ventromedial hypothalamus. The hypothesis was put forward that depression of the fear response after administration of angiotensin II is connected with changes in cortico-subcortical relations, during which ascending activating influences of the mesencephalic reticular formation on the cerebral cortex are abolished due to descending influences of cortical and thalamic neurons.
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PMID:Angiotensin II as a factor inhibiting the fear response. 360 Oct 59

Systemic administration of angiotensin II (ANG II) (200 micrograms/kg sc) to the rat induced a hypothermic response that was characterized within 12 min by a reduction in the rate of O2 consumption, vasodilation of the tail, and a 1.3 degrees C fall in colonic temperature. Administration of ANG II in doses ranging from 10 to 200 micrograms/kg resulted in a decrease in colonic and an increase in tail skin temperature. Angiotensin I (ANG I) (200 micrograms/kg sc) induced a similar hypothermic response which was abolished by pretreatment with the ANG I-converting enzyme inhibitor, captopril (35 mg/kg ip). The interaction of ANG II with cholinergic and adrenergic pathways was evaluated to determine possible mechanisms. Treatment with ANG II (200 micrograms/kg sc) and propranolol, a beta-adrenoceptor antagonist (6 mg/kg ip), resulted in a greater depression of colonic temperature (Tco) than was observed with ANG II alone but did not affect the increase in tail skin temperature (Tsk) accompanying administration of ANG II. When ANG II was administered in combination with the beta-adrenergic agonist, isoproterenol (50 micrograms/kg ip), Tco remained at control levels, whereas an enhancement of the ANG II-induced increase in Tsk occurred. Administration of ANG II in combination with atropine sulfate (6 mg/kg ip), a muscarinic receptor antagonist which crosses the blood-brain barrier, significantly reduced the extent of the fall in Tco without affecting the increase in Tsk. The combined treatment of ANG II and the quaternary analogue, atropine methyl nitrate (3.25 mg/kg ip), which does not cross the blood-brain barrier, failed to affect the hypothermic responses to ANG II. These results suggest that the hypothermic responses to ANG II may be mediated through a central cholinergic pathway and possibly influenced by an adrenergic component. The inability of both adrenergic and cholinergic blockers to affect the vasodilatory response of the tail of the rat to administration of ANG II suggests that the mechanisms subserving heat production can be blocked independently of those subserving heat loss.
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PMID:Angiotensin II-induced hypothermia in rats. 388 74

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.
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PMID:Drinking induced by injection of angiotensin into the rain of the rat. 432 23

Antihypertensive polar renomedullary lipid (APRL), a conglomerate of 1-0-alkyl-2-acetoyl-glycero-3-phosphocholine analogs, ws tested in 4- to 6-week-old spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats using microcirculatory techniques. APRL (0.5 ug/ml), when added to the solution bathing the cremaster muscle, caused significant changes in the diameter, red blood cell velocity, and blood flow in both groups of rats, for arterioles and venules. Arteriolar changes in diameter were significantly greater (p less than 0.05) in SHR than in WKY. Micropipette application of APRL indicated a dose-dependent response for arterioles and venules in both groups. Moreover, the potent nature of this compound was demonstrated. Relative potency of APRL given intravenously was tested in 10- to 12-week-old SHR and WKY. The response curve was shifted significantly to the left for SHR (p less than 0.01). APRL interaction with known controllers of blood flow was tested in SHR. Blockade of cholinergic, beta-adrenergic, or histaminergic receptors did not inhibit APRL action. blockade of prostaglandin or bradykinin synthesis did not prevent depression of blood pressure by APRL. APRL (40 ug/kg) inhibited (p less than 0.001) the pressor response to norepinephrine (1-10 ug/kg) but not to angiotensin II (4 ug/kg). The present study provides direct evidence that APRL is a vasodilator with increased potency in SHR hypertension. The acute vascular response may be mediated by alpha-adrenergic antagonism.
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PMID:Analogs of phosphatidylcholine: alpha-adrenergic antagonists from the renal medulla. 611 27

Effects of octapeptide angiotensin II (AII) were tested on cortical neurons of rat's cerebellum by means of microiontophoresis. It was observed that AII consistently depressed spontaneous firing of Purkinje cell, whereas other unidentified neurons were unaffected. When tested against responses of Purkinje cell to depressant putative neurotransmitters, namely, GABA, glycine, taurine, 5-hydroxytryptamine and noradrenaline, it was observed that AII specifically enhanced depressant action of GABA, while the responses to other substances were unaffected. Both AII-induced depression of cell firing and the AII-induced enhancement of GABA depression were antagonized by a specific GABA antagonist, bicuculline methochloride. We therefore suggest that AII exerts an inhibitory action on Purkinje cells through its modulatory action on bicuculline-sensitive GABA receptors.
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PMID:Angiotensin II-induced depression of Purkinje cell firing and possible modulatory action on GABA responses. 615 37

Hormonal and mean arterial pressure (MAP) responses to posture, isometric handgrip, angiotensin II (AII), adrenocorticotrophic hormone (ACTH), and metoclopramide (MCP), a dopamine (DA) antagonist, were examined in nine men with essential hypertension and nine age- and weight-matched normotensive men on a constant 100 mEq sodium and 80 mEq potassium intake before and after 4 days of administration of the DA agonist, bromocriptine (BEC; 2.5 mg three times a day). BEC depressed supine basal MAP in the hypertensives, and decreased MAP response to posture and isometric exercise in both groups. Hypertensives displayed greater (p less than 0.01) NE responses to posture and exercise than the normotensives. BEC decreased the NE response to 10 minutes of upright posture and exercise more in hypertensives (p less than 0.01) than in normotensives, but following BEC, the responses were similar. BEC did not affect basal PRA or PRA responses to posture and exercise in the two groups. PA responses to ACTH and MCP were similar in both groups, but the hypertensives displayed greater (p less than 0.01) PA responses to AII. BEC suppressed PA responses to AII (p less than 0.01) and to high dose ACTH (p less than 0.05) to a similar extent in both groups. The prolactin as well as the PA response to DA antagonism with MCP was similar in the two groups. These results suggest that dopaminergic control of NE secretion may be altered in essential hypertension. Blood pressure lowering effects of BEC in patients with essential hypertension may be related, in part, to depression of sympathetic nervous system activity.
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PMID:Dopaminergic modulation of pressor and hormonal responses in essential hypertension. 627 98

Earlier studies by other investigators have shown that acute exposure of cultured endothelial cells to hypoxic atmospheres inhibits the activity of the angiotensin converting enzyme in situ, resulting in severe but reversible depression of the rate of degradation of bradykinin. We exposed primary cultures of endothelial cells from the pulmonary artery of the pig to a range of hypoxic gas mixtures and measured the activity of the angiotensin converting enzyme in situ using angiotensin I as substrate. Each cell flask was exposed in random sequence to both hypoxic gas mixtures (PO2 29-69 torr) and room air for 40 min in Dulbecco's medium containing angiotensin I at concentrations of 1000 (N = 7), 500 (N = 8) or 100 ng/ml (N = 4). Angiotensin I disappearance rates and angiotensin II generation rates were linear. Recovery of immunoreactive peptide as either angiotensin I or II following 40 min of incubation was 86 +/- 17% (S.D.). The rate of increase in angiotensin II concentration in surface medium in room air experiments was 91 +/- 51 (S.D.) ng x ml-1 x hr-1. During hypoxia it was 85 +/- 42 ng x ml-1 x hr-1. The difference in rates was not significant by paired t analysis. The results of this study are consistent with earlier observations by the authors which suggest that hypoxia-induced depression of angiotensin I conversion in vivo is due to hemodynamic phenomena. Further studies are needed to clarify the role of cellular mechanisms in hypoxia-induced depression of angiotensin metabolism.
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PMID:Effect of hypoxia on the conversion of angiotensin I to II in cultured porcine pulmonary endothelial cells. 630 52

In experiments lasting 8 h, low (0.5 mg kg-1) or medium (5 mg kg-1) subcutaneous doses of the angiotensin-converting enzyme inhibitor captopril were mildly dipsogenic in sham-operated rats, much more so in rats subjected to bilateral ureteric ligation and not at all in bilaterally nephrectomized rats. Rats with ligated ureters drank enough water to gain weight during the experiments. All other groups lost weight. The enhanced responsiveness of rats with ligated ureters, despite fluid retention, shows that captopril-induced drinking was not secondary to increased renal fluid loss. Ureteric ligation alone which caused some increase in renin secretion was mildly dipsogenic compared with sham operation. Captopril caused further increases in plasma renin concentration and more drinking suggesting that the captopril response is renin-dependent. The failure of the nephrectomized rat to drink after captopril also shows that the response is renin-dependent. The highest dose (50 mg kg-1) of captopril did not at first stimulate drinking, though water intake increased later. Slowness to drink was not the result of general depression of behaviour since drinking in response to subcutaneous hypertonic NaCl or intracranial angiotensin II was not inhibited by the highest dose. Slowness to drink after the highest dose was attributable to blockade of converting enzyme centrally as well as peripherally. This meant that the increased circulating angiotensin I resulting from peripheral blockade of converting enzyme was only slowly converted to angiotensin II in the brain. When cerebral conversion of angiotensin I was prevented by a single intracranial injection of 25 micrograms captopril, drinking in response to the lower doses of captopril was also inhibited in normal rats and in rats with ligated ureters. The same intracranial dose of captopril also inhibited drinking in response to intracranial injections of renin or angiotensin I, but not angiotensin II. The time course of inhibition of renin-induced drinking was similar to that of inhibition of subcutaneous captopril-induced drinking. In conclusion, subcutaneous captopril causes increased water intake through activation of the renal renin-angiotensin system, an effect that is enhanced when the system has already been partly activated by ureteric ligation. Increased circulating angiotensin I resulting from blockade of peripheral converting enzyme must be converted to angiotensin II in the brain in order to stimulate drinking. Drinking is not the consequence of increased fluid loss.
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PMID:Renin dependence of captopril-induced drinking after ureteric ligation in the rat. 635 61

Superfusion of rat anterior pituitary cell aggregates with 10-min pulses of 0.1-10 nM angiotensin II (AII) resulted in a prompt and concentration-dependent rise of PRL release. The effect could be blocked by saralasin, an AII receptor antagonist. The response to AII, but not that to TRH, was rapidly desensitized: a 10 nM AII pulse caused an 80% depression of the response to a subsequent 10 nM pulse given 50 min later. The data provide a possible functional significance for the renin-angiotensin system recently demonstrated in the anterior pituitary.
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PMID:Stimulation of prolactin release by angiotensin II in superfused rat anterior pituitary cell aggregates. 641 Feb 99

The resistance arteries supplying individual exchange villi of the full-term human fetal placenta were examined for their reactivity to various prostaglandins (PG's) as well as for their ability to synthesize biologically active PG's. PGA1, PGF2 alpha, PGE2 and PGE1 produced dose-dependent contractions between 10(-7) and 10(-5)M. The order of potency observed was PGA1 approximately PGF2 alpha greater than PGE2 greater than PGE1. TXB2 was without activity in this preparation. Prostacyclin (PGI2) produced a dose-dependent relaxation of pre-contracted strips between 10(-8)M and 10(-5)M. Arachidonic acid (A.A.) produced stable dose-dependent contractions (10(-5) M to 10(-3)M) which were totally abolished by pretreatment with 10(-7)M meclofenamate (MF). At no concentration of A.A. was any evidence of vascular relaxation observed. Larger concentrations of MF (greater than 10(-6)M) resulted in a non-specific depression of the placental vascular smooth muscle. Meclofenamate (10(-7)M) pretreatment of strips subjected to dose-response studies using PGF2 alpha, PGE2, bradykinin (B K) and angiotensin II (AII) revealed a significant reduction in tension developed to both BK and AII. This finding suggests that the vasoactive peptides BK and AII stimulate the synthesis of vasoconstricting PG's in the fetal placental resistance arteries which relax in response to PGI2 and contract in response to the other PG's tested.
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PMID:The actions of prostaglandins and cyclo-oxygenase inhibition on the resistance vessels supplying the human fetal placenta. 679 96


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