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M Hallbäck-Nordlander

Publications and source records attributed to M Hallbäck-Nordlander.

14 recordsLinked to original sources
PubMed1985

Effect of felodipine on renal hemodynamics and excretion in the dog.

The effects of felodipine on renal hemodynamics and excretion were evaluated in the anesthetized dog. Unilateral renal arterial infusion of felodipine produced ipsilateral increases in the absolute and fractional excretion of sodium and water which were greater than those of potassium; these effects occurred in the absence of changes in mean arterial pressure, renal blood flow, or glomerular filtration rate. There were no significant effects on renal hemodynamic or excretory function in the contralateral kidney. The unilateral renal arterial infusion of isotonic saline or vehicle produced no significant effects on renal hemodynamic or excretory function in either ipsilateral or contralateral kidney. Felodipine, a calcium antagonist with vasodilator antihypertensive properties, in doses which do not affect systemic or renal hemodynamics in the dog, increased urinary flow rate and sodium excretion by decreasing renal tubular water and sodium reabsorption. As a vasodilator antihypertensive agent, felodipine possesses potentially advantageous diuretic and natriuretic properties.

Animals↗
PubMed1984

Cardiovascular studies in rats with respect to some functional and structural relationships of relevance in hypertension and ordinary aging.

Five current lines of cardiovascular studies in rats are outlined, mainly dealing with some functional and structural relationships of particular relevance for hypertension and ordinary aging: 1. Characteristics of the smooth muscles and their neurogenic control in 'Windkessel' arteries, conduit arteries, precapillary resistance vessels and venous capacitance vessels from normotensive rats (WKY) with comparisons to rats with primary hypertension (SHR). 2. Different types of structural renovascular adaptation, comparing aging with advancing SHR hypertension, with 'high-pressure' and 'low-pressure' kidneys in one-clip, two-kidney renal hypertension, and with hypertrophied kidneys in uni-nephrectomized normotensive rats. 3. Relationships between 'structural autoregulation', wall distensibility, vascular reactivity and smooth muscle sensitivity in SHR and WKY hindquarter resistance vessels along with aging. 4. Relationships between wall thickness, luminal dimension and contractility in left ventricles from SHR and WKY during aging, and when one-clip, two-kidney hypertension is superimposed. 5. Interference with the capacity of the neurohormonal mechanisms counteracting blood loss in rats when on chronic low-salt diet.

Aging↗
PubMed1983

Structurally based changes of renal vascular reactivity in spontaneously hypertensive and two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uninephrectomized and intact normotensive rats.

Renal vascular beds from spontaneously hypertensive rats (SHR) at different stages of hypertension, from two-kidney, one-clip renal hypertensive rats (RHR) and from uninephrectomized rats (UNR) were in constant-flow, paired perfusions compared with kidneys from normotensive control rats (NCR) concerning vascular smooth muscle sensitivity to noradrenaline (NA) and resistance vessel reactivity, as reflected by the position, respectively the shape, of the dose-resistance response curves. None of these kidney variants differed significantly from controls concerning smooth muscle sensitivity to NA during in vitro perfusion. However, both the steepness and maximal pressor responses of the renal resistance curves increased progressively with age in SHR, to become ultimately much enhanced when related to age-matched controls. It suggests a well preserved smooth muscle contractility and a progressive elevation of the average wall/lumen ratio in the SHR renal resistance vessels. Also the untouched, "high-pressure" RHR kidneys showed increased vascular reactivity, while it was somewhat reduced in the clipped, "low-pressure" RHR kidneys and unchanged in the hypertrophied but normotensive UNR kidneys. These results, when combined with other findings concerning renal vascular design (Göthberg & Folkow 1982a), illustrate how the renal resistance vessels readily adapt structurally to hypertension, hypotension, kidney hypertrophy and also with age, and in directions which tend to chronically "autoregulate" glomerular blood supply and filtration.

Age Factors↗
PubMed1982

Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats.

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a rightward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at normotensive' or 'hypertensive' levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.

Animals↗
PubMed1982

Performance of the hypertrophied left ventricle in spontaneously hypertensive rats. Effects of adrenergic stimulation.

The performance of isolated hearts from adult male spontaneously hypertensive rats (SHR) and matched normotensive controls (NCR) was investigated in an antegrade perfusion system, where preload and afterload could be varied independently. During electrical pacing of the heart to constant heart rate, increases in afterload, but not in preload, considerably raised cardiac contractility, measured as left ventricular max dP/dt. At afterloads equalling their respective in vivo ones, max dP/dt was similar in SHR and NCR. This indicates that the SHR hearts by myocardial hypertrophy are so well adapted to their raised afterload that an increased inotropic state of the heart is not required. Upon adrenaline addition, SHR and NCR did not differ concerning either "chronotropic sensitivity", i.e. per cent increase in heart rate of the spontaneously beating heart or in "inotropic sensitivity", measured as increase in max dP/dt. However, in this in vitro situation adrenaline increased stroke volume only when the hearts worked at reduced inotropism, induced by lowered temperature (30 degrees C). At maximal inotropic stimulation by adrenaline and occluded outflow, the SHR hearts produced higher systolic pressures than the NCR ones. This reveals an increased maximal contractile capacity of the hypertrophied SHR left ventricle, rather than a reduced one as sometimes suggested.

Animals↗
PubMed1982

Influence of amygdala lesions on cardiovascular responses to alerting stimuli, on behaviour and on blood pressure development in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR), and often also humans genetically predisposed to hypertension, exhibit cardiovascular hyperreactivity to alerting stimuli, which derives from limbic-hypothalamic levels and seems important for inducing primary hypertension. It is further known that the limbic amygdala complex normally reinforces emotionally induced defence reactions. The amygdala were therefore bilaterally destroyed in 6 week old SHR, and compared with sham-operated SHR concerning development of hypertension, cardiovascular reactivity to environmental stimuli and explorative behaviour. When related to controls, the arterial pressure elevation was significantly attenuated in the amygdalalesioned SHR, though their pressure was nevertheless raised 40% at 6 months of age. Concerning cardiovascular responsiveness to mild environmental stimuli the groups did not differ; neither concerning explorative behaviour nor in general motor activity. However, the amygdala-lesioned SHR responded decidely less than controls to stressful, fear-inducing stimuli. The amygdala complex may therefore play an important role in aggravating SHR hypertension by reinforcing defence reactions to stressful influences, when such stimuli are at hand. However, according to the present study the amygdala nuclei are not the origin of the centrally determined cardiovascular hyperreactivity, which in SHR seems decisive for inducing hypertension.

Amygdala↗
PubMed1981

Left ventricular hypertrophy improves cardiac function in spontaneously hypertensive rats.

1. The influence of different arterial pressures on the relationship between diastolic filling pressure and stroke volume was studied during pharmacological cardiac nerve blockade in adult, anaesthetized spontaneously hypertensive rats in comparison with matched normotensive Wistar--Kyoto rats. 2. Peak stroke volumes, obtained by rapid blood volume expansion were similar in both types of rat, despite a more than 40% higher mean arterial pressure in the spontaneously hypertensive rats. 3. When peak stroke volumes were compared in the two groups at equal 'normotensive' or 'hypertensive' arterial pressures, they were always greater in the spontaneously hypertensive rats. 4. Calculation of diastolic wall/lumen ratios indicated that the increase of maximal stroke work in the spontaneously hypertensive rats closely matched the hypertrophic increase in wall/lumen ratio of the left ventricle. 5. These results indicate that left ventricular hypertrophy in established primary hypertension is a physiological adaptation to match left ventricular performance to the raised afterload.

Animals↗
PubMed1980

Left/right ventricular weight ratio: an estimate of 'cardiac adaptation to hypertension'.

1. Left and right ventricular weights were determined in newborn, 6, 15 and 28 week-old spontaneously hypertensive and normotensive control rats. 2. Left and right ventricles were heavier in all spontaneously hypertensive rats than in age-matched control rats, but the left/right ventricular weight ratio was increased only in 15 and 28 week-old spontaneously hypertensive rats. 3. If the cardiomegaly in newborn spontaneously hypertensive rats, in which the two ventricles have worked in parallel until birth, is an adaptation to hypertension in utero, left ventricular weight would rapidly increase after birth as the left ventricle alone is then exposed to an increased pressure. As left/right ventricular weight ratio was not increased in 6 week-old spontaneously hypertensive rats, factors other than hypertension may stimulate cardiac growth in the foetal spontaneously hypertensive rat. 4. This implies an initial structural 'resetting' of the cardiovascular dimensions in spontaneously hypertensive rats and that true pressure-dependent adaptation further potentiates these alterations in cardiovascular structure once hypertension is initiated.

Aging↗
PubMed1979

Haemodynamic alterations after reversal of renal hypertension in rats.

1. Cardiac output, heart rate and mean arterial pressure were determined in two-kidney Goldblatt hypertensive rats of 4 weeks' duration, in matched normotensive controls and in declipped renal hypertensive rats 2 h-28 days after renal artery declipping. 2. After declipping mean pressure fell rapidly due to a corresponding reduction in total peripheral resistance, this being normalized after 1 day. Cardiac output and heart rate remained initially unchanged, but 1 day after declipping the former was significantly increased compared with output in renal hypertensive rats. 3. The initial normalization of total peripheral resistance must be ascribed to a subnormal vascular smooth muscle tone. The reason is that the hypertensive structural vascular changes are not yet significantly reduced and their presence implies an elevated flow resistance, even when vascular smooth muscle activity equals that in normotension. 4. This considerable 'overshoot' in vascular relaxation and lack of reflexogenic tachycardia, despite resetting of baroreceptors, suggest that peripheral as well as central mechanisms contribute to the rapid normalization of mean arterial pressure in two-kidney Goldblatt hypertension in rats, later stabilized by reversal of structural vascular changes.

Animals↗
PubMed1979

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats.

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.

Animals↗
PubMed1979

Performance of the hypertrophied left ventricle in spontaneously hypertensive rat. Effects of changes in preload and afterload.

Isolated hearts from adult spontaneously hypertensive rats (SHR; Okamoto 1969), with established hypertension, were investigated in an antegrade perfusion apparatus where preload and afterload could be varied independently. Frank-Starling curves were constructed at constant afterloads ranging from 50 mmHg to 150 mmHg. As earlier reported, the SHR hearts exhibited a rightward shift of their Frank-Startling relationships compared to those from the normotensive control hearts, though visible only at afterloads up to about 100 mmHg. At higher afterloads the SHR hearts performed significantly better then the NCR ones as their maximal stroke volume was significantly greater compared to that of controls. Thus, left ventricular hypertrophy obviously increases the work capacity of the heart, though at the cost of an altered Frank-Startling relation dependent on the reduced diastolic compliance. For such reasons the myocardial hypertrophy in established SHR hypertension must be considered a physiologic adaptation and not a degenerative phenomenon, though naturally degenerative processes may later become superimposed.

Animals↗