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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of treatment with intravenously administered Angiotensin II (AT II) on blood flow in normal and malignant tissues was investigated clinically. The time course of the effect of AT II was directly recorded by laser doppler velocimetry (LDV) via a probe placed on the surface of normal and malignant tissues. Intravenous administration of AT II resulted in an approximate 3.5 (1.3-14.0)-fold increase in blood flow in eleven malignant tissues, such as breast cancer with direct extension to the skin and abdominal skin metastasis of gastric adenocarcinoma. On the other hand, the blood flow in normal skin was decreased under AT II-induced hypertension, but a reactive hyperemia-like increase was observed soon after the withdrawal of AT II. These results strongly suggested that intravenously administered AT II can act as an adjuvant to enhance, by varying degrees, drug delivery to tumor tissue in cancer chemotherapy and that the administration of chemotherapeutic agents is undesirable soon after the withdrawal of AT II.
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PMID:[Continuous measurement of tumor blood flow under hypertension induced by angiotensin II--clinical studies with laser Doppler velocimetry]. 294 27

Since it was previously reported that atrial natriuretic factor (ANF) may exert an inhibitory effect on renin release, the existence of an Angiotensin II (Ang II)-ANF feedback mechanism was investigated. Male rats were infused intraperitoneally for 7 days with either saline, a nonpressor dose of Ang II (200 ng/kg/min), or a pressor dose (800 ng/kg/min) of Ang II. Systolic blood pressure, plasma ANF, 24-hour urinary sodium excretion, urine volume, and water intake were measured. A significant increase in plasma ANF was observed in the group with a pressor response (blood pressure rose from 89.0 +/- 3.9 to 136.7 +/- 11.4 mm Hg; ANF rose from 36.8 +/- 4.9 to 92.7 +/- 17.7 pg/ml). There was no significant time effect on 24-hour sodium excretion, urine volume, and water intake in both Ang II-infused groups. In a second set of experiments, male rats were infused intravenously for 60 minutes with either saline, a nonpressor dose of Ang II (16 ng/kg/min), or a pressor dose (800 ng/kg/min) of Ang II. Left ventricular end-diastolic pressure, right atrial pressure, and mean arterial pressure were monitored. There was a significant increase in plasma ANF and left ventricular end-diastolic pressure only with the pressor dose (blood pressure rose from 85.0 +/- 6.1 to 140.0 +/- 5.5 mm Hg; ANF rose from 22.6 +/- 6.0 to 108.3 +/- 47.7 pg/ml; left ventricular end-diastolic pressure rose from 5.3 +/- 5.7 to 20.8 +/- 7.9 mm Hg). No significant modification of right atrial pressure was recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Jun
PMID:Atrial natriuretic factor release by angiotensin II in the conscious rat. 296 8

To assess the effects of vasopressors on plasma levels of immunoreactive atrial natriuretic factor (ANF), 13 normal men were studied on two occasions. On the experimental day, subjects received sequential 15-minute intravenous infusions of angiotensin II in doses of 4, 8, and 16 pmol/kg/min. Following a 30-minute recovery period, subjects received sequential 15-minute infusions of phenylephrine in doses of 0.4 and 0.8 micrograms/kg/min. Right atrial pressure, mean pulmonary capillary wedge pressure, pulmonary artery pressure, mean systemic arterial pressure, and plasma levels of renin activity, aldosterone, angiotensin II, and immunoreactive ANF were obtained sequentially throughout the protocol. During the control day, vehicle was infused and plasma samples were obtained for hormone measurements. Infusion of angiotensin II and phenylephrine increased mean systemic arterial pressure in a stepwise fashion. Both right atrial pressure and pulmonary capillary wedge pressure increased significantly during both doses of phenylephrine, but only the highest dose of angiotensin II significantly increased atrial pressures. Plasma levels of immunoreactive ANF increased parallel with the changes in right atrial pressure and pulmonary capillary wedge pressure, with significant increases occurring only at the highest dose of both pressors. Angiotensin II and aldosterone levels increased and renin activity decreased during infusion of angiotensin II. There were no significant changes in plasma levels of immunoreactive ANF during the control day. These studies demonstrate that infusion of vasopressors increases plasma levels of ANF, but only when the vasopressor effect is associated with significant increases in right atrial and pulmonary capillary wedge pressures. Atrial stretch is the most likely mediator of the increase in plasma levels of immunoreactive ANF during vasoconstriction.
Hypertension 1988 Jul
PMID:Effect of vasopressors on atrial natriuretic factor and hemodynamic function in humans. 296 72

The effect of angiotensin II-induced hypertension on selected biochemical parameters was studied in Sprague-Dawley rats. Angiotensin II infusion at rates of 41.7 micrograms h-1 kg-1 and 12.5 micrograms h-1 kg-1 for 2, 5, 10 and 15 days elevated the systolic blood pressure from 143 +/- 7 mmHg to 215-230 mmHg (P less than 0.001) and 185-195 mmHg (P less than 0.001), respectively. The left ventricular weight/body weight ratio increased 10-14% (P less than 0.05) and 23-32% (P less than 0.001) after 2-15 days in rats treated at the lower and higher infusion rates, respectively. Prolyl 4-hydroxylase (PH) activity, a marker of collagen synthesis, was evenly distributed in the left ventricle. PH activity increased by about 100% in both subendocardial and subepicardial layers of the left ventricular wall after angiotensin II infusion for 10 days at 41.7 micrograms h-1 kg-1, but remained unaltered at 12.5 micrograms h-1 kg-1. No change was observed in hydroxyproline concentration. Myosin isoenzymes (V1-V3), which reflect myocardial contractility, were unevenly distributed in the left ventricular wall: the proportion of the fast-turnover isoenzyme (V1) was smaller in the subendocardial layer than in the subepicardial layer. The proportion of V1 decreased after treatment in both layers. Alkaline phosphatase activity, a marker of capillary density, was evenly distributed transmurally in the left ventricular wall. Angiotensin II caused a slight decrease in this activity in both myocardial layers. The results suggest that the elevation of blood pressure leads to transmurally evenly distributed changes in biochemical parameters reflecting collagen synthesis, capillary density and contractile properties of the myocardium.
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PMID:Transmural distribution of biochemical markers of total protein and collagen synthesis, myocardial contraction speed and capillary density in the rat left ventricle in angiotensin II-induced hypertension. 297 33

Angiotensin II stimulated the breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the generation of inositol trisphosphate (IP3) in cultured rat aortic smooth muscle cells. The decrease in PIP2 and increase in IP3 levels were rapid (measurable at 5 seconds; maximum IP3 levels at 15 seconds). The time course of these changes was comparable to that of angiotensin II-induced increases in cytosolic free calcium, as measured by the calcium-sensitive fluorescent indicator quin 2. The IP3 formation was not stimulated by the calcium ionophore A23187 (5 microM), nor were angiotensin II-induced changes in IP3 formation inhibited by the removal of extracellular calcium with EGTA. Angiotensin II appears to be capable of generating more IP3 than is required for maximal release of intracellular calcium. These data are consistent with the hypothesis that generation of IP3 plays a role in the angiotensin II-induced mobilization of calcium from intracellular storage sites in vascular smooth muscle cells.
Hypertension
PMID:Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle. 298 20

Angiotensin II, the biologically active component of the renin-angiotensin system, acts throughout the body to produce an impressive number of cardiovascular, endocrine, metabolic, and behavioral effects. Major actions include elevation of arterial pressure, stimulation of aldosterone secretion, and a variety of effects on the kidneys, brain, and pituitary. Investigation of the role of the renin-angiotensin system in physiological regulation has been greatly facilitated by the availability of specific inhibitors of the formation or actions of angiotensin II, most notably converting-enzyme inhibitors and angiotensin receptor antagonists. Studies with these agents have clearly shown that the renin-angiotensin system plays an important role in the defense of body balance and blood pressure in hypovolemic state, including sodium deficiency and hemorrhage. The inhibitors also lower blood pressure in some forms of hypertension, and converting-enzyme inhibitors are proving to be effective antihypertensive agents.
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PMID:The renin-angiotensin system and body function. 299 6

Angiotensin II and CRF are but two of the several regulatory peptides which exert specific actions in the brain that are complementary with their peripheral effects upon end organs such as the anterior pituitary and adrenal glands. In the pituitary, the two peptides act in a coordinate manner on the corticotroph to regulate ACTH release. In the adrenal gland, angiotensin II receptors are abundant in the zona glomerulosa but are also present in the medulla, where the occurrence of CRF receptors and actions on catecholamine release reveals an additional site at which the two peptides exert related actions, in this case in the peripheral neuroendocrine system. Within the brain, the mapping of AII and CRF binding sites by topical autoradiography has provided new information about the distribution and potential functions of receptors for the two peptides. The central receptors for AII are distributed in a characteristic pattern in brain regions concerned with drinking, regulation of adrenergic function and arterial blood pressure, and control of pituitary hormone secretion. Thus, in addition to its recognized modulatory effects in the peripheral adrenergic system, angiotensin II may be involved in the central control of catecholamine release and action. A central action of AII on the release of regulatory peptides such as vasopressin and CRF, both of which are present in neurones of the paraventricular nucleus, is indicated by the high concentration of AII receptors in this region. Also, the high density of AII receptors in the median eminence suggests that AII modulates the hypothalamic secretion of neuropeptides such as CRF by actions at their site of release, as well as on the cell bodies of neurones responsible for peptide synthesis. The highly localized pattern of AII receptors at numerous specific sites in the brain differs from the more general distribution of many other CNS receptors, and reflects the selective actions of AII on discrete neural systems that subserve precisely integrated functions within the central nervous system. The widespread distribution of CRF receptors, with prominent localization in the cortical and limbic regions, is consistent with the more general neuroregulatory actions of CRF in the brain, and with the presence of immunoreactive CRF in several regions of the brain including the cortex, limbic system, and centers involved in the control of autonomic function. The cortical and limbic receptors are clearly relevant to the effects of centrally administered CRF on both behavioral and visceral responses, with prominent autonomic changes including increased catecholamine release and hypertension.
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PMID:Brain receptors for hypothalamic hormones. 303 94

Angiotensin II (ANG II) has been postulated to have pathogenetic role in diminished glomerular function in a number of animal models of acute renal failure. The present studies were designed to test the hypothesis that modest elevations in circulating ANG II potentiate the ability of ANG II to reduce glomerular capillary surface area through an effect on ANG II binding to glomerular mesangial cells and/or influences on other modulators of function. Rat glomeruli isolated by a sieving technique were employed in vitro in an ANG II radioreceptor assay. Subpressor infusion of ANG II for 36 hours in rats increases the affinity and number of ANG II binding sites of isolated glomeruli. The ability of ANG II to influence function was tested by assessing its effect on glomerular surface area in vitro by image-analysis microscopy, a method of measuring mesangial cell contractility. The sensitivity and magnitude of ANG II-induced decrements in glomerular surface area were increased. ANG II infusion diminished glomerular prostaglandin E2 (PGE2) production, increased basal cyclic adenosine 3',5'-monophosphate (cAMP) production, and enhanced ANG II-induced decrements in cAMP production. In control glomeruli, only pharmacological concentrations of ANG II inhibited cAMP, but after ANG II infusion, physiological concentrations of ANG II were capable of inhibiting cAMP by as much as 57% (below basal values). In conclusion, continuous infusion of subpressor concentrations of ANG II in rats enhances the contractile response of the glomerular mesangial cell through effects on the cell's surface receptor for ANG II and on prostaglandin and cAMP production. These actions may be important mediators of the effects of ANG II on glomerular function associated with a number of experimental models of kidney disease.
Hypertension 1987 Jun
PMID:Subpressor infusions of angiotensin II alter glomerular binding, prostaglandin E2, and cyclic AMP production. 303 6

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect, it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these would be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:The clinical use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 303 14

Angiotensin II-induced hypertension chemotherapy proved to be more effective than conventional chemotherapy using cis-diamminedichloroplatinum (II) (DDP), when applied to an established mouse mammary carcinoma. In an attempt to improve the effectiveness, a cardiotonic such as aminophylline or trans-pi-oxocamphor was added to a solution containing angiotensin II and DDP. A remarkable improvement in therapeutic efficacy was apparent as compared to angiotensin II hypertension chemotherapy. A possible synergism between angiotensin II and the cardiotonic may result in selective delivery of the antitumor drug to the tumor tissue.
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PMID:Some cardiotonics enhance the effectiveness of angiotensin II-induced hypertension cancer chemotherapy in mice. 308 75


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