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Biomedical subjects

F Gross

Publications and source records attributed to F Gross.

At least 91 records · Page 5Linked to original sources
PubMed1981

Changes in renal and urinary kallikrein activity by mannitol-induced osmotic diuresis.

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

Aldosterone↗
PubMed1981

Vasopressin in the plasma of stroke-prone spontaneously hypertensive rats.

1. Plasma concentration of arginine vasopressin, plasma osmolality and packed cell volume were measured in stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto (WKY) rats at different ages. 2. In young and in adolescent SHRSP, at 6, 9 and 12 weeks of age, plasma concentration of vasopressin was diminished as compared with age-matched WKY rats (P less than 0.01), whereas, in 18-week-old rats, the difference was not significant (P greater than 0.05). In contrast, in 24-week-old rats, plasma vasopressin was elevated as compared with WKY rats of the same age (P less than 0.01). 3. In none of the age groups did plasma osmolality differ between the two strains of rats, but in all groups packed cell volume in SHRSP was higher than in WKY rats. 4. During a 48 h period of dehydration, plasma vasopressin concentrations increased similarly in SHRSP and in WKY rats of 6 and 12 weeks of age respectively. 5. It is concluded that vasopressin does not contribute to the development of high blood pressure in SHRSP rats. The reduced plasma concentration of vasopressin may account for the decreased plasma and blood volume and the slightly elevated plasma sodium concentration observed in young SHRSP rats.

Animals↗
PubMed1981

Vasopressin-induced increase in total peripheral resistance in deoxycorticosterone acetate hypertensive rats is buffered by the baroreceptor reflex.

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCa hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 microgram/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA--salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.

Animals↗
PubMed1981

Effects of sodium loading, desoxycorticosterone acetate, and corticosterone on urinary kallikrein excretion.

In male Sprague-Dawley rats, changes in kallikrein activity in urine were produced by high sodium intake (1% saline as drinking fluid for 14 days), and administration of desoxycorticosterone acetate (DOCA, 15 mg/kg s.c. for 5 days), and of corticosterone (2 x 0.2 or 2 x 20 mg/kg s.c. daily for 5 days). Salt loading caused a decrease in urinary kallikrein excretion (p less than 0.005), while DOCA produced an increase (p less than 0.001). While corticosterone, administered in the low dose, had no effect on urinary kallikrein excretion, the high dose, given for 5 days, diminished kallikrein excretion to about half the basal value (p less than 0.001). Simultaneously, the excretion of aldosterone decreased to about one third the amount measured in the corresponding control rats.

Aldosterone↗
PubMed1981

The renal kallikrein-kinin system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. Missing relationship between antidiuretic hormone and the renal kallikrein-kinin system.

The activity of the renal kallikrein-kinin system was investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI); Long-Evans rats (LE) were taken as controls. In the rats with DI, urinary kallikrein excretion was lower (P less than 0.05) than in the LE rats. However, when related to total renal mass or to body weight, there was no difference between the two strains. Kallikrein activity in the renal cortex was similar in the Brattleboro and the LE rats. Antidiuretic hormone (vasopressin tannate) in a dose of 100 mU given once daily for 3 days had no effect on urinary kallikrein excretion in either of the strains. Water deprivation for 24 h resulted, also in both strains, in a similar reduction in urinary kallikrein excretion. The renal kallikrein-kinin system of LE rats and that of DI rats does not principally differ in basic activity, nor in response to the administration of vasopressin, nor to water deprivation.

Angiotensin II↗
PubMed1981

Studies on the direct vasodilator effect of hydralazine in the isolated rabbit renal artery.

In contrast to other large arteries commonly used in organ bath studies, the rabbit renal artery is highly sensitive to the vasodilator action of hydralazine. Helical strips contracted by 10(-7) M norepinephrine started to relax at a threshold concentration of 3.9 x 10(-8) M hydralazine (IC10). The IC50 was 1.4 x 10(-7) M, and at 3 x 10(-6) M hydralazine, the preparations had relaxed almost completely. The development of relaxation was slow, lasting up to 1 hr. Dose-response curves to norepinephrine in the presence of hydralazine were shifted to the right in parallel fashion at an only slight reduction of the maximum response. Contractions of rabbit renal artery strips induced by 45 mM, KCl, or by 10(-7) M norepinephrine superimposed on the KCl-induced tone, were almost unresponsive to hydralazine. Similarly, prolonged incubation of the arterial strips with 10(-5) M ouabain abolished the response to hydralazine probably as a result of a ouabain-induced depolarization. Neither indomethacin, an inhibitor of tissue prostaglandin synthesis, nor sulpiride, an antagonist to dopamine, interfered significantly with the vasodilator action of hydralazine. This suggests that the relaxant effect of hydralazine is not mediated by locally formed prostaglandins and that it is not dopaminergic in nature. The present findings indicate that hydralazine is a potent direct vasodilator with a predominant action on pharmacomechanical coupling but little effect on electromechanical coupling.

Animals↗
PubMed1980

Reversal of corticosterone-induced supersensitivity of vascular smooth muscle to noradrenaline by arachidonic acid and prostacyclin.

In the isolated perfused hindlimb preparation of rats treated with corticosterone (2 x 20 mg/kg daily for 2 days), the dose-response curve to noradrenaline was shifted to the left, indicating supersensitivity of the vascular bed to noradrenaline. Perfusion with arachidonic acid (10(-5) M) and prostacyclin (10(-9) M) for 5 min reversed the supersensitivity induced by corticosterone. The metabolite of prostacyclin, 6-keto PGF1 alpha(10(-9) M), was ineffective in this respect. In rats which had received desoxycorticosterone acetate (2 x 5 mg/kg daily for 7 days), there was supersensitivity of the hindlimb preparation to noradrenaline similar to that in corticosterone-treated rats. In that case, however, administration of arachidonic acid did not reverse the leftward shift of the dose-response curve. Administration of indomethacin (2 x 2.5 mg/kg for 7 days) prior to the perfusion experiment also resulted in a shift of the noradrenaline dose-response curve to the left, which was less pronounced than the shift induced by corticosterone. Combined administration of corticosterone and indomethacin caused the same increase in noradrenaline sensitivity as did corticosterone alone. Since glucocorticoids inhibit the release of arachidonic acid from phospholipids, it is concluded that corticosterone may enhance the sensitivity to noradrenaline by affecting the biosynthesis of prostaglandins.

Animals↗
PubMed1980

Ureteral contractions induced by rat urine in vitro: probable involvement of renal kallikrein.

Rat urine, even at a 1:10 final dilution in Tyrode's solution, stimulates contraction of the ureteral musculature in vitro. This effect can be ascribed to the presence of kallikrein or a kallikrein-like enzyme in urine. Isometric contractions of ureters were prevented by previous addition of aprotinin to the organ bath. Urine also lost its activity after inactivation of enzymes by heat or acid treatment.

Animals↗
PubMed1980

Vasoconstriction and increased blood pressure in the development of accelerated vascular disease.

The pathogenesis of acute vascular lesions has been studied in two types of accelerated vascular disease. Firstly, vascular lesions were induced by a short-term (2 h) infusion of angiotensin II. Low doses of angiotensin II caused only a slight increase in blood pressure and non-destructive lesions. High doses caused a significant elevation of blood pressure and destructive vascular lesions. Secondly, in renovascular hypertension, renal vascular disease was induced by the removal of the stenosing clip from the renal artery. Incidence and severity of destructive vascular lesions were correlated with the calculated gradient between the pressure before and beyond the stenosis. Anaesthesia had a protective effect on the development of destructive vascular lesions in both models. Obviously, this effect is not related to a reduction of the systemic pressure, but rather to the suppression of abnormal vascular tone, characterized by focal constriction alternating with overdilation. Vasomotor changes, which cause a local overdilation, may be responsible for destructive vascular lesions even at normal to subnormal blood-pressure values. Destructive vascular lesions occur as a result of the exceeding of a critical wall tension. The necrosis of medial smooth-muscle cells in non-destructive lesions may be explained by an excessive contraction, which "surpasses" the metabolic capacity of the cells.

Anesthesia↗
PubMed1980

Increased kallikrein excretion in spontaneously hypertensive rats and its inhibition by 6-hydroxydopamine.

Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). "Chemical sympathectomy", induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.

Animals↗
PubMed1980

Plasma catecholamine levels and vascular response in deoxycorticosterone acetate hypertension of rats.

1. In rats with deoxycorticosterone acetate (DOCA) hypertension basal plasma concentrations of noradrenaline and adrenaline correspond to those of sham-treated controls. 2. In DOCA-treated rats frusemide caused a more pronounced increase in plasma noradrenaline than in control rats. This difference was not observed for adrenaline. 3. In the isolated perfused hind-limb preparation the sensitivity to noradrenaline was already enhanced before blood pressure was elevated. 4. These results suggest that the adrenergic vascular tone is increased in DOCA hypertension in rats.

Animals↗
PubMed1980

Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats.

Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.

Aging↗
PubMed1980

Significance of sodium, sympathetic innervation, and central adrenergic structures on renal vascular responsiveness in DOCA-treated rats.

The effects of sodium, sympathetic innervation, and central adrenergic structures on the development of changes in renal vascular reactivity were studied in unilaterally nephrectomized rats treated with a single implant of deoxycorticosterone acetate (DOCA; 100 mg/kg). Vascular reactivity to norepinephrine (NE) and vasopressin (ADH) was assessed in isolated kidneys perfused with a synthetic medium. Influence of sodium was determined by placing DOCA-treated rats on high, normal, and low sodium intakes. Neural influence was studied by means of local denervation of the renal artery and by intravenous (iv) and intraventricular (ivt) administration of 6-hydroxydopamine (6-OHDA). Marked changes in renal vascular reactivity in DOCA-treated rats were already apparent prior to the rise in blood pressure. Dose-response curves for NE and ADH showed parallel leftward shifts and decreased threshold doses. Normal sodium intake, local denervation, and peripheral sympathectomy had no effect on the development of these vascular changes in DOCA-treated rats. However, sodium deficiency and ivt administration of 6-OHDA totally prevented development of enhanced vascular reactivity. These results imply that increased vascular reactivity is a major factor in the development of DOCA-hypertension.

Adrenergic Fibers↗