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PubMed1990

Water intake and changes in plasma and CSF composition in response to acute administration of hypertonic NaCl and water deprivation in sheep.

Water intake and changes in plasma and cerebrospinal fluid (CSF) composition were measured in response to intracerebroventricular (i.c.v.) and intracarotid infusions of hypertonic NaCl solutions and after 48 h of water deprivation in sheep. Significant interindividual differences in dipsogenic sensitivity to i.c.v. NaCl were found, whereas no such differences were observed in response to intracarotid infusion of hypertonic NaCl. In the more sensitive animals, the increase in CSF [Na] at initiation of drinking during i.c.v. infusion did not differ significantly from the increase in plasma [Na] seen at the thirst threshold during intracarotid infusion of 1 M NaCl. The thirst-eliciting infusions of hypertonic NaCl into the carotid arteries were associated with a small, significant, increase in CSF [Na], which however did not differ from that caused by an i.c.v. non-dipsogenic 'control' infusion of a slightly hypertonic (0.154 M) NaCl solution. Water deprivation for 48 h induced increases in CSF and plasma [Na] similar to those observed at the onset of drinking in response to i.c.v. and intracarotid infusions of hypertonic NaCl. However, the dehydrated animals drank about four times the amount of water consumed in response to the separate treatments with hypertonic NaCl. It is concluded that significant interindividual differences in dipsogenic sensitivity to osmotic stimuli are present in sheep, and that these differences may not necessarily be simultaneously expressed on both sides of the blood-brain barrier. The thirst-eliciting effect of intravascular infusion of hypertonic NaCl may be induced without concomitant increase in CSF [Na] and/or osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Evidence for an influence of CSF sodium concentration upon ACTH-mediated cortisol response to intravenous and intracerebroventricular angiotensin II.

The influence of cerebrospinal fluid (CSF) NaCl concentration upon the cortisol release induced by intracerebroventricular (i.c.v.) and intravenous (i.v.) infusions of angiotensin II (AII) was studied in conscious goats. A first series of experiments involved i.c.v. infusion (20 min; 20 microliters min-1) of simply hypertonic (0.5 M) NaCl, or of AII (2 pmol kg-1 min-1) dissolved in 0.5 M or isotonic (0.15 M) NaCl or in isotonic glucose. The most pronounced rise in plasma cortisol concentration (PC) was elicited by AII in 0.5 M NaCl, but responses of nearly the same size were obtained by merely 0.5 M NaCl and by AII in isotonic NaCl, whereas AII in glucose induced a smaller PC rise. An urge to drink developed during all infusions, except during the AII/glucose infusion. Here, however, thirst became apparent 2-6 min post-infusion. When, in a second series, the hypertonicity of the NaCl was reduced to 0.3 M, and the dose of AII to 0.5 pmol kg-1 min-1, only the infusion of AII in 0.3 M NaCl elicited any appreciable rise in PC. The response was approximately the same size as that earlier obtained as the effect of the larger dose of AII dissolved in isotonic saline. In a third series of experiments, a 30-min i.c.v. infusion of isotonic glucose, preceding and out-lasting a 10-min i.v. infusion of AII (40 pmol kg-1 min-1), was found to extinguish the rise in PC obtained as the effect of a separate i.v. infusion of AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1985

Cholecystokinin neuron systems and their interactions with the presynaptic features of the dopamine neuron systems. A morphometric and neurochemical analysis involving studies on the action of cholecystokinin-8 and cholecystokinin-58.

A unique role for CCK-58 compared to that for CCK-8 has been demonstrated in the modulation of central catecholaminergic mechanisms and neuroendocrine functions. It is of paramount importance to localize CCK-58 immunoreactivity within the brain in order to establish if separate CCK-58- and CCK-8-immunoreactive neuron systems exist. The two most significant actions of CCK-58 are a marked lowering of TSH secretion and a selective increase of DA turnover in DA-CCK co-existing synapses in the nucleus accumbens and tuberculum olfactorium.

Animals↗
PubMed1988

Intracerebroventricular bethanechol chloride administration in Alzheimer's disease.

In June 1983 we began evaluating intracerebroventricular (ICV) cholinergic drug infusion in patients with biopsy-documented Alzheimer's disease (AD). An initial trial in four patients showed this treatment approach to be feasible, but objective improvement in cognitive or social function was not documented. A double-blind, placebo-controlled crossover study involving a larger number of patients has since been done. The results of this study, presented here, document a statistically significant improvement in some neuropsychological test results during periods of drug infusion. However, the degree of improvement is not sufficient to justify further treatment with the presently available drug, bethanechol chloride.

Aged↗
PubMed2003

Role of nitric oxide in regulating the rat hypothalamic-pituitary-adrenal axis response to endotoxemia.

This work examines the role of nitric oxide (NO) in the periphery (i.e., on the pituitary) and the brain (particularly on corticotropin-releasing factor [CRF] and vasopressin [VP] neurons in the paraventricular nucleus [PVN] of the hypothalamus) as a modulator of the ACTH response to lipopolysaccharide. We previously showed that NO restricted the pituitary response to VP while it facilitated the synthesis of PVN CRF and VP. In our experience, only relatively high doses of lipopolysaccharide (>50 microg/kg, injected intravenously [i.v.]) cause detectable increases in PVN neuronal activation. Our hypothesis, therefore, was that pituitary NO-VP interactions would predominate in rats injected with a low dose of lipopolysaccharide (0.5 microg/kg, i.v.) while the stimulatory influence of the gas on PVN neuronal activity would play an important role following i.v. injection of a large dose of lipopolysaccharide (50 microg/kg, i.v.). We observed that the ability of 0.5 microg/kg lipopolysaccharide to release ACTH was significantly enhanced by the subcutaneous (s.c.), but not the intracerebroventricular (i.c.v.) injection of L-NAME, an arginine derivative that blocks NO synthesis. The effect of s.c. L-NAME was reversed by immunoneutralization of endogenous VP, which indicated that in this model, the ability of lipopolysaccharide to release ACTH depended, at least in part, on the influence exerted by NO on the pituitary response to VP. In rats injected with the high lipopolysaccharide dose, the s.c. injection of L-NAME decreased plasma ACTH levels compared to those in rats pretreated with the vehicle. The effect of s.c. L-NAME was not significantly altered by VP antibodies. These results indicate that in this model, the primary influence of NO was exerted in the PVN and/or its afferents and that it did not depend on a peripheral, VP-mediated effect of the gas. On the one hand, these data are at odds with our finding that the i.c.v. injection of L-NAME only marginally altered the ACTH response to the large dose of lipopolysaccharide. As i.c.v. injected L-NAME should have primarily decreased hypothalamic, but not pituitary NOS, its only modest influence on ACTH release may have been due to a balance between stimulating and inhibiting effects of NO within the brain. As high doses of lipopolysaccharide increase brain levels of prostaglandin, monoamine, and proinflammatory cytokines, it will be important to investigate the influence exerted by NO on these secretagogues and on their interactions with PVN CRF and VP neurons, which may help us resolve the issues raised by our results. Collectively, these data support our hypothesis that the mechanisms mediating the ACTH response to a low lipopolysaccharide concentration involve the inhibitory VP-mediated influence of NO on pituitary activity. By contrast, the stimulatory effect of high doses of lipopolysaccharide on ACTH release depends, at least in part, on the ability of NO to upregulate PVN neuronal activity.

Adrenocorticotropic Hormone↗
PubMed1982

The effects of changes in osmolality and sodium concentration on angiotensin-induced drinking and excretion in the pigeon.

1. The pigeon drank copiously after a short latency in response to intracerebro-ventricular (I.C.V.) infusion of angiotensin II dissolved in isotonic NaCl. There were small, insignificant increases in urinary excertion so that the increased water intake caused the pigeon to go into positive fluid balance. Water was chosen in preference to 0.3 M-NaCl, which was also available to drink in these experiments.2. I.C.V. infusion of angiotensin dissolved in water, or in isotonic or hypertonic solutions of non-eletrolytes, or in KCl or CaCl(2) resulted in about half the water intake produced by angiotensin dissolved in isotonic NaCl.3. I.C.V. infusion of hypertonic NaCl alone caused drinking. I.C.V. infusion of angiotensin dissolved in hypertonic NaCl caused an amount of water to be drunk that was a simple addition of the amounts drunk in response to angiotensin dissolved in isotonic NaCl and to the extra amount of NaCl.4. Drinking in response to I.C.V. infusion of two other dipsogenic peptides, eledoisin and physalaemin, was similarly affected by the composition of the solutions in which they were dissolved.5. The pigeon also drank in response to intravenous (I.V.) infusion of angiotensin II dissolved in isotonic NaCl. Urine flow and sodium excretion increased markedly so that the pigeons just maintained fluid balance.6. In contrast to the reduction in intake when angiotensin was infused I.C.V. dissolved in hypertonic non-electrolytes, I.V. infusions of angiotensin dissolved in hypertonic non-electrolytes caused enhanced drinking, compared with the corresponding infusions of angiotensin dissolved in isotonic NaCl.7. Drinking induced by I.V. infusion of angiotensin was little affected by simultaneous I.C.V. infusion of isotonic or hypertonic sucrose, or water, but it was increased by simultaneous I.C.V. infusion of hypertonic NaCl.8. Drinking responses were partly additive when angiotensin was given by simultaneous I.C.V. and I.V. infusion.9. The increased urine flow and electrolyte excretion in response to I.V. infusion of angiotensin were little affected by simultaneous I.C.V. infusion of angiotensin.10. These experiments suggest that in the pigeon there may be separate sets of receptors in the cerebral ventricles for initiating drinking, one set responding to angiotensin, another to hypertonic NaCl. Outside the blood-brain barrier, and accessible to blood-borne substances, there may also be separate sets of receptors, one set responding to angiotensin, another to increases in effective osmolality of the blood.

Angiotensin II↗
PubMed1984

Involvement of the renin-angiotensin system in captopril-induced sodium appetite in the rat.

The angiotensin converting enzyme inhibitor, captopril, given to rats in their drinking water (about 40 mg/day) for 6 days caused an increase in intake of hypertonic NaCl solution which began 1-2 days after the captopril was started and reached a plateau after 4-5 days. Twice-daily subcutaneous injections of captopril (15 mg per injection) elicited a sodium appetite similar in pattern to that seen with oral administration. The rats remained in sodium and fluid balance during oral captopril treatment and the haematocrit did not alter. Captopril infused directly into the ventricles (12 micrograms/h), or captopril reaching the brain from the periphery across a leaky blood-brain barrier, suppressed the sodium appetite which normally follows oral captopril. Continuous intravenous infusion of captopril at rates high enough to block angiotensin converting enzyme in the brain (25, 50 or 500 mg/day) did not cause sodium appetite. As soon as the rate was reduced to a low value (5 mg/day), NaCl intake increased. In conclusion, moderate levels of circulating captopril which do not cross the blood-brain barrier in sufficient amounts to block cerebral angiotensin converting enzyme, result in an increase in circulating angiotensin I which stimulates sodium appetite when it is converted to angiotension II in the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Central and peripheral effects of the peptide ANF on renal function and blood pressure in hypertensive rats.

1. The present study assesses renal and blood pressure effects of systemically and intracerebroventricularly (I.C.V.) administered atrial natriuretic factor (ANF) in anaesthetized New Zealand genetically hypertensive (NZGH) rats and their normotensive substrain (NZN). 2. Plasma ANF concentration was significantly raised in NZGH compared with NZN animals. Intravenous ANF administration increased circulating ANF concentration to similar levels in NZGH and NZN rats. Plasma aldosterone concentrations were initially similar in normotensive and hypertensive animals and were reduced markedly by I.V. ANF administration in both groups. 3. Peripheral administration of ANF produced a significant and sustained hypotension during the period of the hormone administration in NZGH animals, while arterial mean blood pressure (MBP) was not altered significantly in NZN rats. Central infusion of ANF produced no change in MBP in either NZGH or NZN animals. There was no detectable change in heart rate during central or peripheral administration of the hormone in either group. 4. By comparison with animals maintained on hormone-free infusate, urine flow changed little over the 80 min period of I.V. ANF infusion in NZGH rats but was markedly increased in NZN animals. Urinary sodium excretion was elevated during ANF infusion in both NZGH and NZN animals. Central infusion of ANF produced a diuresis in NZN rats but a slight reduction in urine flow in NZGH animals, while sodium excretion was not affected in either group. 5. It appears from the present study that central and peripheral ANF effects on renal function and blood pressure differ in hypertensive and normotensive animals. These differences may in part reflect adjustments to long-term elevation in plasma ANF in hypertension and in part are possibly associated with disturbances in related endocrine mechanisms.

Aldosterone↗
PubMed1976

Rifamycin in neonatal flavobacteria meningitis.

Three newborn infants with meningitis due to Flavobacterium meningosepticum were treated with rifamycin administered parenterally and directly into the cerebral ventricles. Antibiotic concentrations of blood and cerebrospinal fluid (CSF) were monitored during treatment. There was rapid sterilization of the CSF after this antibiotic. Jaundice was the only toxicity noted. All 3 infants developed hydrocephalus and are shunt dependent. Two of them are otherwise free of neurological complications and are developing normally. Rifamycin is a safe and effective antibiotic in this form of neonatal meningitis.

Female↗
PubMed1982

Lateral cerebral ventricle and preoptic-anterior hypothalamic area infusion and perfusion of beta-endorphin and ACTH to unrestrained rats: core and surface temperature responses.

Both beta-endorphin and ACTH have been found in high concentrations within the hypothalami of mammals and each neuropeptide has been proposed to play a physiological role in regulating body temperature. In an attempt to determine how these peptides may alter thermoregulation, small, microgram concentrations of beta-endorphin and ACTH were injected either into lateral cerebral ventricle (ICV) or directly into the preoptic-anterior hypothalamic area (POAH) or perfused into the POAH of unrestrained rats. Core (rectal) and surface (tail) temperatures were recorded before and after ICV and POAH injection of 1 microgram of beta-endorphin or ACTH or perfusion (10 ng/microL) of either neuropeptide. POAH perfusion of naloxone HCl following the neuropeptide perfusion was tested to determine the specificity of the temperature responses. Regardless of the route of central administration, beta-endorphin, in the concentrations used, consistently evoked a hyperthermic core temperature response, that could be antagonized by naloxone. Increased core temperatures may, in part, have been due to peripheral vasoconstriction, as suggested by the decreases seen in tail temperature. The same concentrations of ACTH failed to show any prominent core temperature changes. Results suggest that beta-endorphin is a more potent modulator than ACTH in altering core temperatures of unrestrained rats. Whether beta-endorphin and ACTH act physiologically in an antagonistic manner to maintain a constant body temperature remains to be proven.

Adrenocorticotropic Hormone↗
PubMed1989

Involvement of different mechanisms in the stimulatory effects of cholecystokinin octapeptide on gastrointestinal and colonic motility in dogs.

The effects of an intravenous infusion of cholecystokinin octapeptide (CCK-8, 1 microgram.kg-1.h-1) were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Attempts to antagonize the increase of motility appearing at the three levels during CCK infusion were made using different blockers to elucidate the mechanisms involved. Asperlicin (a specific CCK antagonist) blocked the effects of CCK-8 at the three levels, while atropine and somatostatin were only effective in the jejunum and colon. Methyl-levallorphan (a mu-opiate antagonist that poorly crosses the blood-brain barrier) antagonized the CCK-induced colonic stimulation when intracerebroventricularly administered. Serotonin, histamine, substance P, and K-antagonists as well as a benzodiazepine did not modify the CCK-8 induced stimulation. It was concluded that the stimulatory effect of CCK-8 resulted from (a) a direct stimulation of the smooth muscle cells at gastric level, (b) a cholinergic activation of the jejunum and the colon, and (c) the involvement of a mu-opioid central component in the colonic response only.

Animals↗
PubMed1977

Effect of angiotensin II and glucocorticoids on plasma angiotensinogen concentration in the dog.

The increase in plasma angiotensinogen concentration produced by angiotensin II infusion in the dog is accompanied by an increase in plasma corticosteroid concentration and is prevented by adrenalectomy. The present study was undertaken to test the possibility that the angiotensinogen response to angiotensin is mediated via an increase in glucocorticoid secretion. Infusion of angiotensin II (3-6 mug/h for 5 h) into the third cerebral ventricle of five dogs increased plasma corticosteroid concentration from 3.5+/-0.6 to 11.8+/-1.5 mug/dl (P less than 0.025) but did not increase plasma corticosteroid concentration from 2.7+/-0.4 to 7.8+/-1.5 mug/dl (P less than 0.05) but again failed to increase plasma angiotensinogen concentration. On the other hand, more prolonged glucocorticoid treatment with dexamethasone produced a significant increase in plasma angiotensinogen concentration within 24 h. Intravenous infusion of angiotensin II (50 mug/h for 5 h) in five acutely hypophysectomized dogs receiving a cortisol infusion caused only a small increase in plasma corticosteroid concentration (5.0+/-0.5 TO 6.9+/-0.6 mug/dl, P less than 0.02) but increased plasma angiotensinogen concentration from 967+/-122 to 1,358+/-204 ng/ml (P less than 0.02). These results indicate that although glucocorticoids can increase plasma angiotensinogen concentration, the angiotensinogen response to angiotensin II is not dependent on increased glucocorticoid secretion.

Adrenal Cortex Hormones↗
PubMed1985

Hypertension during chronic peripheral and central infusion of angiotensin III.

Recent studies have suggested that the angiotensin II (ANG II) metabolite [Des-Asp]ANG II (ANG III) may be nearly equipotent with the parent compound in causing several acute neural responses known to be stimulated by angiotensin peptides (i.e., drinking, augmentation of sympathetic neurotransmission, and centrally mediated pressor responses). Because neural actions of ANG II are thought to contribute importantly to the ability of this hormone to cause chronic hypertension, the purpose of the present experiments was to explore the cardiovascular effects of chronic administration of ANG III either into the bloodstream or directly into the brain via the cerebral ventricles. The neurogenic component of the pressor response to acute infusion of ANG III also was reinvestigated. In anesthetized pithed rats (n = 6) ANG III had only 10% of the pressor potency of ANG II when given by acute (5-10 min) intravenous infusion. In conscious rats (n = 5) ANG III had 25% of the pressor potency of ANG II when tested using acute intravenous administration. The acute intravenous pressor potency ratio in conscious versus pithed rats was 4.8 for ANG III and 1.1 for ANG II, suggesting that, compared with ANG II, the pressor response to ANG III shows a greater dependence on neurogenic mechanisms at the doses tested. Chronic (5-day) intravenous infusion of ANG III (at 10, 20, and 100 ng/min) caused sustained hypertension without changes in fluid/electrolyte balance, but only at a dose (100 ng/min) estimated to produce blood levels of ANG III well beyond the "physiological" range.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2002

Gastric protective effect of peripheral PYY through PYY preferring receptors in anesthetized rats.

The influence of intravenous peptide YY (PYY) on the gastric injury induced by 45% ethanol was investigated in urethane-anesthetized rats. PYY (25, 75, 125, and 250 pmol x kg(-1) x h(-1)) significantly reduced gastric lesions by 36, 59, 40, and 38%, respectively. Antibody against ratPYY (2 mg/rat) injected intravenously completely prevented the gastroprotective effect of intravenous PYY (75 pmol x kg(-1) x h(-1)), whereas injected intracisternally (460 microg/20 microl), it significantly prevented intracisternal PYY (24 pmol/rat)-induced 58% reduction of ethanol lesions but not that induced by intravenous PYY. Vagotomy did not influence the gastroprotective effect of intravenous PYY. The Y(1)/"PYY-preferring" receptor agonist [Pro(34)]PYY (75 pmol x kg(-1) x h(-1) iv) significantly decreased ethanol-induced gastric lesions by 82%, whereas [Leu(31), Pro(34)]NPY, a Y(1)/Y(3) agonist, and PYY-(3-36), a Y(2) agonist, had no effect. These data indicate that PYY-infused intravenously at doses reported to mimic postprandial peak blood levels prevents ethanol-induced gastric injury through vagal independent pathways and PYY-preferring receptors.

Animals↗
PubMed2004

Gastrointestinal satiety signals IV. Apolipoprotein A-IV.

The focus of this article is to review evidence that apolipoprotein A-IV (apo A-IV) acts as a satiety factor. Additionally, information regarding the general involvement of apo A-IV in the regulation of food intake and body weight is stated. Apo A-IV is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and liver secrete apo A-IV, but the small intestine is the major organ responsible for circulating apo A-IV. There is now solid evidence that the hypothalamus, especially the arcuate nucleus, is another active site of apo A-IV expression. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and does not appear to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, the local formation of chylomicrons acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine (PYY). The inhibition of food intake by apo A-IV is mediated centrally. The stimulation of intestinal synthesis and secretion of apo A-IV by lipid absorption are rapid; thus apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight, as it is regulated by both leptin and insulin. Chronic ingestion of a high-fat diet blunts the intestinal as well as the hypothalamic apo A-IV response to lipid feeding. It also suppresses apo A-IV gene expression in the hypothalamus. Whereas it is tempting to speculate that apo A-IV may play a role in diet-induced obesity, we believe the confirmation of such a proposal awaits further experimental evidence.

Animals↗
PubMed1998

Effect of cerebroventricular perfusion of bombesin on gastrointestinal myoelectric activity.

The effect of intracerebroventricular (i.c.v.) perfusion of bombesin (BBS) on the interdigestive migrating myoelectric complex (MMC) activity was examined in conscious dogs with electrodes implanted on the stomach and small intestine. Cannulas and a catheter were chronically positioned in the lateral and fourth cerebral ventricles, respectively. i.c.v. perfusion of BBS, which failed to increase plasma BBS levels, replaced phase I activity in the stomach and duodenum by intense irregular spike activity and decreased the occurrence rate of MMCs, whereas intravenous infusion of BBS evoked phase II-like activity, mainly in the jejunum and ileum, and suppressed phase III activity. These data suggest that the effect of i.c.v. administration of BBS was mediated by direct activation of central brain structures. During i.c.v. perfusion of BBS, cycling in plasma levels of motilin persisted even when phase III activity was absent and plasma levels of epinephrine rose significantly. Epinephrine infusion, however, did not affect myoelectric gastrointestinal activity except for prolonging phase II. Thus it is unlikely that the central action of BBS is exerted by motilin or epinephrine.

Animals↗
PubMed1995

Losartan improves baroreflex control of heart rate of coarcted hypertensive rats.

To assess the role of angiotensin (ANG) II in both the increased heart rate (HR) and the impaired baroreceptor reflex control of HR that characterize the chronic phase of coarctation hypertension (CH), we compared basal HR, mean arterial pressure (MAP), and baroreflex sensitivity of coarcted hypertensive rats treated chronically with losartan, captopril, or vehicle. Baseline HR was recorded daily, and MAP and reflex HR changes and plasma renin activity (PRA) were measured in coarcted and sham-coarcted rats on the 5th day after coarctation. Both captopril (10 mg.kg-1.day-1 po) and losartan (10 mg.kg-1.day-1 po) caused a small nonsignificant reduction of hypertension (132 +/- 5 and 133 +/- 5, respectively, vs. 147 +/- 9 mmHg in vehicle-treated rats), but equally inhibited the late tachycardic phase (-37 +/- 13 and -29 +/- 12 beats/min in captopril- and losartan-treated groups, respectively, vs. +79 +/- 19 beats/min in vehicle treated rats). Similar results were obtained for other groups of coarcted hypertensive rats after suppression of PRA by bilateral nephrectomy. Although hypertensive levels were the same during both treatments, only losartan given orally or intracerebroventricularlly (1.25 micrograms.kg-1.h-1) was effective in improving the reflex bradycardia. The depressed reflex tachycardia was corrected by chronic oral treatment with losartan. The data suggest that the tachycardia occurring in the chronic phase of CH is mediated by blood-borne ANG II and that the normalization of the reflex control of HR by losartan is achieved by blockade of type I receptors of ANG II in central areas accessible to oral or centrally administered losartan but not to oral captopril.

Administration, Oral↗