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Biomedical subjects

D F Bohr

Publications and source records attributed to D F Bohr.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effects of felodipine on blood pressure and lymphocyte membrane characteristics in spontaneously hypertensive stroke-prone rats.

Adult spontaneously hypertensive stroke-prone rats (SHRSP) and age- and sex-matched Wistar-Kyoto rats (WKY) were treated with the calcium-channel antagonist felodipine for 2-4 weeks (1 mg/g in rat chow powder). Control rats of both strains were fed untreated chow. At the end of the treatment period we measured blood pressure, net potassium efflux and intralymphocytic calcium concentration. In the untreated rats the values for these parameters were significantly higher in SHRSP than in WKY. Felodipine treatment caused a reduction in the SHRSP values to WKY levels. We conclude that the high blood pressure of SHRSP results from an increase in membrane permeability to calcium. The resultant increase in intralymphocytic calcium concentration causes an increase in net potassium efflux via calcium-activated potassium channels. By reducing the membrane permeability to calcium with felodipine, these parameters were returned to normal or near-normal levels.

Animals↗
PubMed1988

The influence of potassium and bicarbonate on red blood cell sodium in the DOCA-hypertensive pig.

The effects of plasma potassium, and blood bicarbonate on red blood cell sodium were studied in vivo in seven pigs implanted subcutaneously with DOCA (100 mg/kg) impregnated in Silastic. Mean arterial pressure, red blood cell sodium, plasma sodium, plasma potassium, and blood bicarbonate were measured from 5 days pre-implant to 30 days post-implant. One day post-implant, the pigs had significant increases in mean arterial pressure and red cell sodium content, and a significant decrease in plasma potassium concentration. In KCl infusion studies when plasma potassium was raised an average of 2.13 +/- 0.17 mEq/L, red blood cell sodium fell 0.61 +/- 0.10 mEq/L cells. When blood bicarbonate was raised 6.9 mEq/L by infusing NaHCO3, red blood cell sodium increased 0.79 mEq/L cells. The changes in red blood cell sodium were rapid, occurring within one hour after either of these plasma electrolyte shifts. We conclude that either plasma potassium or blood bicarbonate, or both, can serve as regulators of red blood cell sodium content in vivo, and cause the elevated level of red blood cell sodium that we have found in the DOCA-hypertensive pig. If these plasma electrolyte changes cause a similar increase in intracellular sodium in vascular smooth muscle or in a blood pressure regulating center in the brain, they may play a role in producing the arterial pressure elevation of mineralocorticoid-induced hypertension.

Animals↗
PubMed1988

Parallel effects of DOCA on salt appetite, thirst, and blood pressure in sheep.

Salt appetite was quantified in sheep by measuring the relative amounts of high-salt (266 meq/kg) and low-salt (6 meq/kg) pelleted alfalfa that they ate. Given a choice of these two foods, normal sheep ate twice as much low-salt as high-salt pellets. Following DOCA administration the sheep rapidly developed an increased salt appetite, and after 10 days they ate approximately three times as much high-salt as low-salt pellets. Their choice rapidly reverted to control values after the end of the DOCA treatment. The changes in salt appetite were accompanied by changes in thirst and mean arterial pressure. We hypothesize that these effects of DOCA reflect changes that parallel those this mineralocorticoid causes in the hypothalamic regulatory centers for salt appetite, thirst, and blood pressure.

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PubMed1988

Cell membrane permeability in hypertension.

A great deal of evidence has been presented which suggests that a generalized increase in cell membrane permeability to various ions is a fundamental defect associated with hypertension. In addition, some of the evidence is supportive of a central role of this defect in the pathogenesis of hypertension. The source of this defect may lie in the reduced calcium binding capacity of the cell membrane. Because of this reduced capacity the membrane is less stable and is more permeable to various ions.

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PubMed1987

Genetic relationship between a lymphocyte membrane abnormality and blood pressure in spontaneously hypertensive stroke prone and Wistar-Kyoto rats.

The fluxes of sodium and potassium across the lymphocyte membrane in spontaneously hypertensive, stroke prone rats (SHRSP) are greater than those in Wistar-Kyoto rats (WKY). In order to define the relationship of these abnormal membrane traits to arterial pressure elevation, their distributions were studied in F1, F2, and backcross progeny of the cross of SHRSP and WKY rats. In the F1 generation, arterial pressure and potassium efflux values resembled those of the WKY parents suggesting that these traits are dominant in the normotensive rat; sodium influx values resembled those of the SHRSP parents. There was poor correlation (r = 0.45) between blood pressure and sodium influx in the F2 generation. There was a high correlation between blood pressure and potassium efflux (r = 0.86), suggesting that these two traits may be under the control of a common genetic mechanism.

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PubMed1987

Cerebral vascular responsiveness in deoxycorticosterone acetate-salt hypertensive rats.

Alterations in cerebral vascular responsiveness were investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Initial studies on the passive-force response characteristics of strips of basilar artery revealed no difference between control and DOCA-salt rats. No difference in acetylcholine-induced relaxation was seen between the two groups. The contractile response to KCl was similar in control and DOCA-salt rats. An increase in both threshold and midrange sensitivities to serotonin (5-HT) was seen in basilar artery from DOCA-salt rats. However, extracellular Ca sensitivity in the presence of 10(-6) M 5-HT was not altered. Intracellular Ca release (phasic contraction in response to 10(-6) M 5-HT) was similar in control and DOCA-salt rats. Relaxation in response to Ca (membrane stabilization) was also not different. Whereas sodium nitroprusside (SNP)-induced relaxation was not altered in basilar artery from DOCA-salt rats, a significant decrease in isoproterenol (ISO)-induced relaxation was observed. Relaxation following washout of maximal contractions to KCl and 5-HT was similar in the two groups. These results demonstrate specific alterations in cerebral vascular responsiveness of DOCA-salt rats. Whereas KCl contractile and SNP relaxation responses were not affected, responses to 5-HT and ISO were significantly altered. These changes do not appear to be related to alterations in the endothelium or in the Ca responsiveness of the vascular smooth muscle.

Animals↗
PubMed1987

Vascular reactivity in the spontaneously hypertensive stroke-prone rat. Effect of antihypertensive treatment.

This study investigated vascular responsiveness in stroke-prone spontaneously hypertensive rats (SHRSP) and the effect of antihypertensive treatment on this responsiveness. Weanling (4-week-old) male and female SHRSP and Wistar-Kyoto rats (WKY) received either the antihypertensive combination treatment of hydralazine plus hydrochlorothiazide in drinking water or tap water alone (controls) for 15 weeks. Whereas the antihypertensive combination prevented the development of hypertension in treated SHRSP (SHRSP-T), blood pressure remained unchanged in treated WKY (WKY-T). Femoral arterial smooth muscle responsiveness to KCl, norepinephrine, and calcium (in the presence of either 40 mM KCl or 1 microM norepinephrine) was not altered in SHRSP when compared with WKY. A significant increase in the sensitivity of femoral arteries to KCl and calcium (in the presence of 40 mM KCl) was seen, however, in SHRSP-T and WKY-T. An increased sensitivity to norepinephrine and calcium (in the presence of 1 microM norepinephrine) was seen only in SHRSP-T. Isoproterenol-induced relaxation was significantly attenuated in both SHRSP and SHRSP-T. Relaxation induced by sodium nitroprusside and calcium (membrane stabilization) was not different between the four groups. These results show that femoral arterial smooth muscle responsiveness to vasoconstrictor stimuli is not altered in SHRSP but that beta-adrenergic-mediated relaxation is attenuated. Antihypertensive treatment resulted in an enhanced responsiveness to these vasoconstrictor stimuli but had no effect on the relaxation properties of femoral arterial smooth muscle.

Animals↗
PubMed1986

Vascular interactions of serotonin and norepinephrine in renal hypertensive rabbits.

Vascular responses to norepinephrine (NE) are potentiated in the presence of serotonin (5-HT) and are attenuated by previous exposure to 5-HT. This study was designed to determine whether alterations in the interactions of these agonists occur in renal hypertension. Helical strips of femoral artery from two-kidney, one clip (2K1C) hypertensive and control rabbits were mounted in muscle baths for isometric force recording. Arterial strips from 2K1C rabbits were more sensitive to 5-HT than were those of control rabbits. The sensitivities of these two groups of vessels to NE were not significantly different. The 5-HT potentiation of NE was present at lower 5-HT concentrations in vessels from 2K1C rabbits than in those from control rabbits. Previous exposure to 5-HT attenuated NE responses of arteries from 2K1C less than it did those of control rabbits. Although 5-HT had little effect on loading of cellular stores of calcium in the resting muscle, previous 5-HT exposure attenuated calcium influx during an NE response, and this attenuation was not as great in vascular smooth muscle from the hypertensive animal as it was in that from the normotensive control. These results indicate that in vascular smooth muscle cells from 2K1C rabbits the potentiating action of 5-HT is increased, due to the increased sensitivity to this agonist, and the attenuating action is decreased due to a greater calcium influx during NE stimulation.

Animals↗
PubMed1986

Calcium-related abnormalities in lymphocytes from genetically hypertensive rats.

We examined the effect of various external calcium concentrations on net potassium efflux and net sodium influx in lymphocytes from spontaneously hypertensive rats (SHR), stroke-prone spontaneously hypertensive rats (SHRSP), and Wistar-Kyoto rats (WKY). Net potassium efflux was greater in lymphocytes from SHRSP than in those from WKY at external calcium concentrations of 0.1, 0.3, 1.0, and 3.0 mM but not at 0 mM (14.9 +/- 0.8 vs 13.0 +/- 0.7 mmol per kilogram of dry weight per hour, respectively). Net sodium influx in lymphocytes from SHRSP was greater than in those from WKY at all external calcium concentrations tested (0, 0.1, 1.0, and 3.0 mM). In contrast to lymphocytes from WKY, net potassium efflux and net sodium influx in lymphocytes from SHRSP were not significantly higher at 0 than at 0.1 mM external calcium concentration. Lymphocytes from SHRSP had elevated intracellular free calcium concentrations (173.6 +/- 7.4 nM, n = 8), as compared with lymphocytes from WKY (98.1 +/- 9.1 nM, n = 8). These data suggest that the interaction of calcium with the lymphocyte plasma membrane directly affects monovalent ion permeability and is altered in lymphocytes from SHRSP, as compared with those from WKY. Our findings support the hypothesis that in hypertension there is a generalized increase in cell membrane permeability to calcium and monovalent ions, which may result from a reduced number of calcium-binding sites on the plasma membrane.

Animals↗
PubMed1986

Immunoreactive atrial natriuretic hormone levels increase in deoxycorticosterone acetate-treated pigs.

Extensive evidence reported here and elsewhere indicates a hormonal role for atrial natriuretic factor. In the light of this evidence, it appears that atrial natriuretic hormone is a more appropriate term for these peptides than atrial natriuretic factor. Plasma levels of immunoreactive atrial natriuretic hormone were measured daily in seven pigs before and 1 week after subcutaneous implantation of deoxycorticosterone acetate (DOCA). Nine other animals underwent daily measurements of mean arterial pressure and central venous pressure during similar treatments. Plasma immunoreactive atrial natriuretic hormone levels rose progressively during the first 3 days after implantation, from a basal level of 60 +/- 9 pmol/L to a peak level of 159 +/- 21 pmol/L (p less than 0.05), and they remained significantly elevated throughout the rest of the 7-day observation period. In two animals that were restudied 6 weeks after DOCA implantation, plasma immunoreactive atrial natriuretic hormone had returned to preimplantation levels. The rise in plasma hormone levels after DOCA implantation closely paralleled the previously reported time course of mineralocorticoid escape. Whether atrial natriuretic hormone plays an important part in the escape phenomenon remains to be determined.

Animals↗
PubMed1986

Calcium and vascular smooth muscle membrane in hypertension.

A major focus of past and recent research in hypertension has been on the characterization of the nature of the vasculature changes which lead to the observed increase in total peripheral resistance responsible for the elevation of arterial pressure. Here we survey recent evidence which suggests that altered handling of calcium is a primary membrane defect in hypertension. Evidence for the primacy of this defect is provided by studies demonstrating a reduced ability of the membrane to bind calcium in diverse tissues from hypertensive animals. The reduced calcium binding ability appears to be responsible for a greater membrane permeability to monovalent and divalent cations. This greater permeability contributes to the increased sensitivity to vasoconstrictor stimuli of vascular smooth muscle in hypertension.

Animals↗
PubMed1985

Functional bases for individualities among vascular smooth muscles.

This review deals with cellular factors that contribute to individualities of vascular smooth-muscle function in different organ systems and at different levels of the vascular tree. Particular attention has been given to: membrane receptors responsive to catecholamines, serotonin, angiotensin II, dopamine, and acetylcholine; membrane properties, including resting and action potentials, and the Na+, K+ ATPase electrogenic pump; regulation of cellular Ca2+; contractile proteins; metabolism, and cell messengers. Differences in membrane receptors appear to be the major basis for the individualities found in various vascular smooth muscles. Differences in cell-membrane properties and Ca2+ regulation are also significant causes of variability. Cell metabolism and contractile proteins contribute relatively less to the individualities of vascular smooth muscle. Too little is known about cell messengers to assess their contribution to this individuality.

Animals↗
PubMed1985

Increased sensitivity of the osmotic control of vasopressin in sheep with deoxycorticosterone acetate-induced hypertension.

The development of hypertension induced by deoxycorticosterone acetate (DOCA) in sheep was accompanied by increases in both the plasma concentration and the urinary excretion of vasopressin. The vasopressin response to an osmotic stimulus (i.v. infusion of 0.85 mol NaCl/l at 4 ml/min for 75 min) was studied before and after the development of hypertension induced by DOCA in six sheep. Before DOCA implantation, the osmotic stimulus resulted in an increase of plasma osmolality (POSM) from 290 +/- 1 to 303 +/- 1 (S.E.M.) mosmol/kg H2O and in plasma vasopressin concentration (PAVP) from 0.23 +/- 0.04 to 1.07 +/- 0.15 microunits/ml. At least 30 days after DOCA implantation when mean arterial blood pressure had risen from 81 +/- 3 to 117 +/- 5 mmHg, the same osmotic load caused an increase in POSM from 290 +/- 2 to 298 +/- 2 mosmol/kg H2O and PAVP from 0.45 +/- 0.05 to 2.02 +/- 0.27 microunits/ml. POSM and PAVP were significantly correlated in every experiment. However, the slope of the relationship increased significantly (P less than 0.01) after the animals had developed hypertension (0.185 +/- 0.026 vs 0.070 +/- 0.011 (microunits vasopressin/ml)/(mosmol/kg H2O]. The intercepts were similar. After the DOCA implant had been removed osmotic sensitivity returned to normal.

Animals↗
PubMed1985

Composition of glycosaminoglycans from aortas from deoxycorticosterone-induced hypertensive pigs.

Hypertension was induced in young male pigs by subcutaneous implantation of deoxycorticosterone acetate in a Silastic rubber carrier. Hemodynamic variables were periodically monitored. Six to eight weeks after implantation, the animals were necropsied and aortas were dissected. Glycosaminoglycans (GAG) were isolated from aortas from hypertensive pigs and from normotensive controls. Individual glycosaminoglycans in mixtures were fractionated and quantitated by chromatography on Dowex 1 Cl- column. No differences were noted in total glycosaminoglycan concentration between hypertensive and control animal aortas; the differences in individual GAG in aorta media-adventitia between the groups were not statistically significant. The relative proportions of heparan sulfate and dermatan sulfate in aorta intima were significantly greater (p less than 0.05) in hypertensive aortas than in normotensive intima. These two glycosaminoglycans increased in hypertensive animals at the expense of chondroitin 4-sulfate and hyaluronic acid. There was no difference in chondroitin 6-sulfate between the groups. A possible explanation of changes of glycosaminoglycans in hypertension because of altered lysosomal activity is suggested.

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