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D Susić

Publications and source records attributed to D Susić.

At least 19 recordsLinked to original sources
PubMed1996

[The effect of captopril on the development of adriamycin nephropathy in rats with spontaneous arterial hypertension].

The effects of captopril on morphologic changes and clinical course of adriamycin (ADR) nephropathy in spontaneously hypertensive rats (SHR) were examined. After ADR infections rats were divided into two groups: ADR-C group (n = 20) given captopril (60 mg/kg per day) and ADR group (n = 19) receiving no antihypertensive treatment. SHR were examined every 6 weeks. Captopril normalized systemic blood pressure, but failed to prevent proteinuria. It slowed down renal function deterioration in the early stage of ADR nephropathy (weeks 6 and 12), but at the end of the study both groups had the same degree of renal failure irrespectively of whether blood pressure was well controlled with captopril or hypertension persisted. Captopril slowed down mesangial expansion in the early stages of ADR nephropathy, but at the end of the study there was no statistically significant difference between these two groups. Treatment with captopril also reduced the development of glomerular sclerosis.

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PubMed1995

Factors affecting the ability of the renal medulla to exert an antihypertensive function.

To examine whether changes in renomedullary osmolality and the activity of the renin-angiotensin system may influence the ability of the renal medulla to exert an antihypertensive function, rats were exposed to several manoeuvers. These affected either the medullary osmolality or the renin-angiotensin system (salt or saccharose load, salt depletion, treatment with captopril alone or in combination with salt depletion). A comparison of the antihypertensive capacity of the renal medulla was studied by transplanting renal medullae from the various groups into one-kidney one-clip hypertensive rats. A significant and quantitatively similar reduction in blood pressure was observed in hypertensive rats that received transplants of the medullae from control, salt or saccharose loaded rats and captopril treated rats. In contrast, medullae from salt depleted rats did not affect blood pressure when transplanted into hypertensive animals. The addition of captopril restored the antihypertensive function of renal medulla in salt depleted rats. The results do not support the view that osmolality of the renal medulla regulates its antihypertensive capacity, and suggest that angiotensin II may restrain renomedullary antihypertensive function.

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PubMed1989

Megakaryocytopoiesis in spontaneously hypertensive rats (SHR).

Bone marrow megakaryocytes and their progenitors were studied in SHR in order to obtain more information about megakaryocytopoiesis in hypertension since it is known that various anomalies of platelet function occur in hypertension. Megakaryocytopoiesis under steady state conditions and following stimulated erythropoiesis and thrombocytopenia was not found to be significantly different in SHR from that in normotensive Wistar controls.

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PubMed1988

The role of the renal medulla in blood pressure control.

It is well established that the renal medulla exerts a potent endocrine-like antihypertensive action. The purpose of this paper is to summarize the data that define the extent to which the renomedullary antihypertensive action is involved in blood pressure regulation. It appears that in animals kept under physiological conditions, the renal medulla is not necessary for the maintenance of normotension, since its destruction does not usually result in hypertension. However, in animals exposed to hypertensive stimuli, the presence of renomedullary tissue appears to be the key factor in resisting the increase in blood pressure. Evidence is presented to show that inherited or acquired deficiency of renomedullary antihypertensive function may contribute to the development of various forms of hypertension. It is suggested that inherited differences in the antihypertensive capacity of the renal medulla may account for differing sensitivities of various strains of animals to hypertensive stimuli. Finally, data are presented to show that renomedullary deficiency induced by a decrease in renal perfusion pressure, which could be a consequence of hypertensive damage to renal vessels, may contribute to the increase in blood pressure in various forms of hypertension.

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PubMed1988

Dependence of the hypertensive effect of chronic vanadate administration on renal excretory function in the rat.

The effect of vanadate, an agent that in rats exerts potent vasoconstrictor and diuretic action on blood pressure, cardiac output, total peripheral resistance and plasma and extracellular fluid volume, was investigated in normal rats and in rats with diminished renal excretory function. In normal rats, chronic dietary vanadate did not affect blood pressure, but induced an increase in total peripheral resistance and a decrease in cardiac output, plasma and extracellular fluid volume. In rats with diminished renal excretory function, vanadate increased blood pressure and total peripheral resistance without affecting cardiac output, plasma and extracellular fluid volume. The results indicate that this agent, with predominant vasoconstrictor action, does not cause sustained hypertension unless renal excretory function is diminished.

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PubMed1988

Pulmonary artery pressure in rats with hereditary platelet function defect.

Pulmonary vasoactivity of several biochemical components produced or stored in platelet was the justification for the study of pulmonary artery pressure in fawn-hooded rats (FHR) with hereditary platelet storage pool deficiency. Anesthetized (pentobarbital 35 mg kg-1 i.p.) FHR had higher right ventricular systolic pressure compared with normal Wistar rats (NWR) matched in sex and age (57.7 +/- 6.8 vs. 34.8 +/- 1.2 mm Hg; p less than 0.01). The incidence of higher pulmonary artery pressure (greater than means + 2 SD of NWR) was 68% among FHR. A significant difference was recorded between FHR and NWR in the relative weight of the right ventricle (0.092 +/- 0.021 vs. 0.048 +/- 0.001 g/100 g; p less than 0.05). Rise in pulmonary artery pressure in FHR after 4 weeks of normobaric hypoxia was found to be comparable to that seen posthypoxically in NWR. Morphological consequences of pulmonary hypertension, ranging from moderate medial hypertrophy of small arteries to muscularization of pulmonary arterioles, were recorded in about 50% of FHR with increased pulmonary artery pressure.

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PubMed1988

Erythrocytosis in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SH) with an increased number of red blood cells (RBC), microcytosis, and normal hemoglobin (Hb) concentration were used to study the effect of different manipulations of the erythron on erythropoietin production and on erythroid progenitor proliferation by bone marrow cells in order to gain insight regarding the regulation of erythropoiesis. The serum erythropoietin (Ep) level was increased in untreated SH rats. After stimulation by either bleeding, hemolysis, or acute hypoxia, both the erythropoietin level and erythroid colony-forming unit (CFU-E) proliferation by bone marrow cells increased in SH rats to levels that were similar to those of normotensive Wistar (W) rats. Exposure to chronic hypoxia induced an increase in Hb concentration in SH rats concomitantly with the increase in RBC. The results obtained in SH rats raise the possibility of a defect in nonEp stimulators of erythropoiesis that may alter Hb synthesis.

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PubMed1986

Effect of chronic vanadate administration on pulmonary circulation in the rat.

The effect of prolonged dietary vanadate administration on pulmonary hemodynamics was investigated. Rats treated with vanadate for 2 months developed pulmonary hypertension, as indicated by significantly (p less than 0.001) higher mean and systolic right ventricular pressure. Cardiac output was not affected by vanadate administration, while the calculated pulmonary vascular resistance was found to be significantly (p less than 0.05) higher in rats treated with vanadium. Right ventricular hypertrophy was also noted in vanadium-treated animals. Vanadium treatment did not significantly affect systemic circulation. The results indicate that vanadium administration induces pulmonary hypertension.

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PubMed1985

Platelets in rats with chronic normobaric hypoxic pulmonary hypertension.

A study of the platelet count in rats exposed to normobaric hypoxia for 4 weeks revealed that hypoxia alone, without any change in barometric pressure, considerably reduced the number of thrombocytes. In order to elucidate the mechanism of hypoxic thrombocytopenia, the survival and recovery of 51Cr-labelled platelets were tested. The survival and recovery of platelets from hypoxic rats injected into normoxic recipients were normal. However, when 51Cr-labelled platelets from normoxic rats were injected into a hypoxic recipient, the survival was found to be normal but the recovery of those platelets was lower than in the normal rat. This finding suggests that the reduction of platelet counts in normobaric hypoxia may be due to the platelets' partial sequestration.

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PubMed1984

Hemodynamic effects of two ergot derivatives in the conscious spontaneously hypertensive rat.

The effect of acute and chronic administration of two ergot derivatives, dihydroergosine (DHESN) and ergosinine (ESNN), on blood pressure, heart rate, cardiac output and total peripheral resistance was studied in conscious spontaneously hypertensive rats. Acute administration of either DHESN or ESNN (50-100 micrograms/kg) resulted in prompt and significant (p less than 0.01) decrease of both blood pressure and heart rate, which lasted for more than 12 h. The decrease in blood pressure was due to reduction in total peripheral resistance, as cardiac output remained unchanged. Prolonged treatment (50 micrograms/kg, i.p., every second day for 12 days) with either DHESN or ESNN significantly (p less than 0.01) decreased blood pressure. In chronically treated rats, total peripheral resistance was found to be decreased while no changes in cardiac output and heart rate were observed. The results indicate that both DHESN and ESNN are potent antihypertensive agents, due to their vasodilator effects. The hypotensive effect of DHESN could be partially blocked by haloperidol, but not by yohimbine. Both, DHESN and ESNN antagonized the effect of phenylephrine on blood pressure.

Animals↗
PubMed1984

Prostaglandin synthesis inhibitors in erythropoiesis.

PG synthesis inhibitors were used to study the role of PG in modulating Ep effects on erythroid progenitors. The stimulating effect of exogenous Ep on both 59Fe incorporation into RBC and CFU-E number in polycythaemic mice was inhibited with indomethacin and aspirin treatment during the posthypoxic period. The inhibitory effect of indomethacin on CFU-E derived colonies was demonstrated only when cultured bone marrow and spleen cells were obtained from mice stimulated by prolonged exposure to hypoxia. The results implicate the role of PG in the Ep dependent regulation of the erythroid progenitor cell compartment size and Ep responsiveness in vivo.

Animals↗
PubMed1983

A sex difference in the hemodynamic effects of chronic normobaric hypoxia in rats.

The packed cell volume was higher and the increase in systolic pressure in the right ventricle, as an indication of systolic pressure in the pulmonary artery, was smaller in female rats previously exposed for 4 weeks to normobaric hypercapnic hypoxia, as compared to males treated in the same way. Gonadectomy performed in male rats either on the first day of life or after maturation did not have a significant influence on circulatory reaction to chronic normobaric hypoxia. Female rats in permanent estrus and those with ovariectomy had larger posthypoxic hypertrophy of the right ventricle as indicated by higher values for right/left ventricular weight ratio and relative weight of the right ventricle, than untreated controls.

Animals↗
PubMed1981

Decreased pulmonary pressor response to acute hypoxia in chronically hypoxic rats.

The pulmonary vascular response to an acute hypoxic stimulus was examined in rats which were kept for 4 weeks in a hypoxic environment and compared to that of rats kept in a normoxic environment. To this end, the effects of breathing gas mixtures containing 7, 21 an 100% O2 on right ventricular systolic pressure (RVPs), cardiac output (Q) and calculated pulmonary vascular resistance (PVR) in chronically hypoxic (CH) rats and rats kept in a normoxic environment (N) were examined. During breathing of 21% O2 RVPs, Q, and PVR were all higher in CH than in N rats. Breathing a gas mixture containing 7% O2 had no effect on systemic blood pressure, heart rate or Q, in both CH and N rats. When compared to breathing of 21% O2, the RVP and PVR remained unchanged in CH rats breathing 7% O2, while both variables significantly (p less than 0.01) increased in N rats. The presented data indicate that the reaction of the pulmonary vasculature to an hypoxic challenge is decreased in CH rats.

Animals↗
PubMed1980

Role of the renal medulla in the resistance of rats to salt hypertension.

The role of the renal medulla in the sensitivity of rats to the hypertensive stimulus of salt overload was investigated in a strain of rats shown to be resistant to salt hypertension. Rats were divided into four groups: I -2/3 nephrectomy (medulla left intact); II - unilateral nephrectomy plus dissection of the medulla of the remaining kidney (UNDRM);III - UNDRM plus renomedullary autotransplantation; IV - UNDRM plus renocortical autotransplantation. Two weeks after surgery all rats were given 1% NaCl solution instead of drinking water, and the blood pressure was measured every week for 6 weeks. The blood pressure, although increased, was significantly lower in groups I and III than in the other two groups throughout the period of salt loading. Renal excretory function was similarly altered in all rats, as indicated by similar plasma creatinine concentrations. The results indicate that antihypertensive activity of the renal medulla may account for the high resistance of the described rat substrain to salt hypertension.

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PubMed1980

Dynamics of regression of right ventricular hypertrophy in rats with hypoxic pulmonary hypertension.

Normobaric hypoxia caused a significant increase in right/left ventricular weight ratio in rats, a reliable indicator of hypertrophy of the right ventricle, already after 1 week of intermittent hypoxic confinement 7 days after termination of a 4-week hypoxic exposure the right/left ventricular weight ratio was significantly lower compared to the values immediately after hypoxic treatment. 8 weeks of sojourning in a normoxic environment were not sufficient to normalize the right ventricular systolic pressure and right/left ventricular weight ratio. It is concluded that changes in the right ventricular mass in rat is a fast reaction to the changes in pressure load.

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