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Biomedical subjects

B Folkow

Publications and source records attributed to B Folkow.

At least 19 recordsLinked to original sources
PubMed1992

Influence of the renal medulla and early treatment with enalapril upon the development of hypertension in young spontaneously hypertensive rats.

OBJECTIVE: To investigate the role of the renal medulla in early hypertension in spontaneously hypertensive rats (SHR), and to explore whether the attenuated increase of pressure induced by enalapril treatment is affected by chemical medullectomy. DESIGN: Forty-four male SHR were studied from 5 to 18 weeks of age: 22 remained intact; 22 were medullectomized at 5.5 weeks of age with 2-bromoethylamine hydrobromide; 11 of each of these two groups were treated with enalapril from 6 to 12 weeks of age. Blood pressure, heart rate and body weight were recorded intermittently, and at 18 weeks renal function was also analysed. RESULTS: The results indicate a protective effect of the renal medulla against severe pressure rises in SHR, although even when enalapril also lowered blood pressure in medullectomized SHR, persistent improvements of glomerular filtration rate and renal flow conductance occurred only in intact SHR. Furthermore, after enalapril treatment ended blood pressure rose to higher levels in medullectomized SHR, despite greater sodium-water losses. CONCLUSION: The renal medulla seems to exert a protective role both during and after enalapril treatment.

Animals↗
PubMed1992

Trophic effects of hypophyseal hormones on resistance vessels and the heart in normotensive and renal hypertensive rats.

UNLABELLED: Arterial pressure is an important determinant of cardiovascular structure and relates positively to it. The purpose of this study was to determine whether pituitary hormones influence the relation of pressure and structure. Male Sprague-Dawley rats, aged 5 weeks, were studied in three groups: the first underwent hypophysectomy; the second was hypophysectomized but received replacement therapy with growth hormone and thyroxine; the third served as controls. Four days later half of each group underwent unilateral renal artery clipping, the other half serving as normotensive controls. For 5 weeks estimates were made of systolic blood pressure, heart rate, body weight and plasma renin activity. Rats were then killed; left ventricular, kidney and adrenal weights were determined and, using hindquarter perfusion, estimates were made of resistance at maximal dilatation (reflecting inner radius), and of maximal pressor response (reflecting wall thickness). RESULTS: (1) Hypophysectomy in non-clipped rats reduced growth rate, systolic blood pressure and heart rate while plasma renin activity rose. As related to pressure and to body weight, resistance at maximal dilatation, maximal pressor response, left ventricular weight remained at the juvenile values of a 5-week-old rat. Hormone replacement restored values to those of control rats aged 11 weeks. (2) Clipping in the control group rats increased systolic blood pressure more than in hypophysectomized and growth hormone and thyroxine receiving hypophysectomized groups even though plasma renin activity remained higher in hypophysectomized than in control rats. Plasma renin activity was highest in hypophysectomized rats with highest pressure. (3) Systolic blood pressure related positively to left ventricle weight, resistance at maximal dilatation, maximal pressor response and calculated wall thickness to inner radius ratios in all groups. However, these regressions were all, like renal structural adaptation, considerably depressed in the hypophysectomized group. Hormone replacement restored the relation of structure and pressure towards that of control group rats. Thus, growth hormone and thyroxine influence maturation of the normal cardiovascular system and greatly enhance its structural upward resetting in hypertension.

Animals↗
PubMed1992

Critical review of studies on salt and hypertension.

The importance of salt intake for blood pressure homeostasis is critically surveyed, from a physiological point of view. Both ordinary rats and the great majority of mankind appear to tolerate quite a wide range of intakes at only minor effects on blood pressure. Further, both species seem to have their "physiological setpoints" at closely similar levels, if only differences in body size and metabolic rate are considered. No doubt risks increase towards both end of the intake spectrum, where those at low intakes have been much neglected though they were recently explored in rats, also concerning the mechanisms involved. In both species, however, genetic differences affect also the salt balance, where a minority of human beings shows various degrees of "salt sensitivity", apparently more often so in e.g. American blacks than in whites. This may well reflect a relative dominance for mechanisms favouring salt conservation which, in some environments, seems to be of vital importance. However, when such individuals are confronted with the more liberal salt consumption in modern society, their particular setting of salt balance may rather serve to aggravate or even precipitate hypertension, especially when other predisposing elements are at hand. It is tentatively discussed how to best handle such situations without interfering too much with consumption habits and "quality of life" for the great majority of "salt resistants"; further that more research should be directed towards identification and further analyses of salt sensitive subgroups.

Animals↗
PubMed1992

Effect of chronic ethanol consumption upon cardiovascular reactivity, heart rate and blood pressure in spontaneously hypertensive and Wistar-Kyoto rats.

OBJECTIVE: Clarification of the effect of chronic ethanol consumption upon cardiovascular reactivity in rats. DESIGN: Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) normotensive rats were randomly allocated in groups of 10 to ethanol in tap water [20% (v:v) after the first week or tap water for 7-12 weeks]. METHODS: Intra-arterial blood pressure and heart rate were measured at rest and in response to vibration and noise stress. Vascular reactivity was assessed in isolated paired perfused hindquarters and in mesenteric arterioles in a Mulvany-Halpern myograph. RESULTS: Resting intra-arterial blood pressure but not heart rate was lower in both ethanol-treated groups. The ethanol treatment increased the SHR heart rate response to sudden noise but the WKY response did not increase. Pressor responses to noise were initially greater in the ethanol-treated SHR. The ethanol had no effect upon isolated perfused hindquarter resistance at maximal dilation, dose-response curves in response to noradrenaline or vasopressin, or maximal contractile strength. Isolated mesenteric arterioles showed that ethanol had no effect upon responses to nerve stimulation or upon the 50% effective dose required for a response to noradrenaline or vasopressin. CONCLUSIONS: Ethanol treatment heightened the heart rate reactivity to stress without substantially affecting vascular neuro-effector characteristics in SHR. This is likely to be a central effect, caused by suppression of the central nervous inhibitory systems that influence the heart rate and baroreflex activity in a strain of rat already showing evidence of an impaired ability to modulate the heart rate and blood pressure in response to stress. The small reduction in resting blood pressure may be a consequence of the lower weight in the ethanol-treated rats, and/or may reflect a direct depressing action by the alcohol on vascular and cardiac muscle. These findings are discussed in the context of ethanol-induced hypertension in humans and possible genetic variations in central nervous, cardiac and vascular effects.

Alcoholism↗
PubMed1992

Hypertension and endothelial function--aspects of atheroma protection.

Old concepts of an "inert" vascular endothelium have been entirely discredited. It is now known that the vascular endothelium and media form a "functional unit", communicating via both electric and humoral signals. Normal endothelium maintains vascular dilation through release of various dilatory substances, the main one being endothelial relaxing factor (EDRF), which is nitric oxide (NO). EDRF is, for example, released in response to increased shear stress that accompanies high flow rates, and acts by engaging the cyclic GMP system of smooth muscle cells. Even potential vasoconstrictors such as vasopressin, catecholamines and serotonin release EDRF. Endothelial release of prostacyclin supplements the EDRF action. EDRF (and prostacyclin) also inhibit platelet aggregation. In the presence of hypertension and/or atherosclerosis, endothelial function is often impaired and pressor/thrombogenic factors such as endothelin, thromboxane, vasopressin, catecholamines, and serotonin become more dominant. Antihypertensive therapy should, ideally, seek to restore endothelial function to normal.

Animals↗
PubMed1992

Angiotensin II, vascular structure and blood pressure.

Angiotensin II (Ang II) in low dose raises blood pressure slowly by a mechanism which is not understood, but which is clearly different from the better known direct vasoconstrictor effect. Vascular hypertrophy develops during this slow pressor response, but is not wholly a consequence of the increase of pressure. We discuss non-pressor mechanisms by which Ang II may act as a growth factor to promote structural vascular change. Studies with cultured vascular smooth muscle cells suggest at least three possibilities, but none of these has been tested in vivo during slow pressor infusion of Ang II. The action of growth factors may be important in hypertension since increased arterial pressure causes vascular hypertrophy. Growth factors influence markedly the extent of this hypertrophic response and, however produced, vascular hypertrophy has an important influence on resistance and arterial pressure in hypertension.

Angiotensin II↗
PubMed1991

Giraffes, rats and man--what is the importance of the 'structural factor' in normo- and hypertensive states?

1. The normal structural adaptation of heart and vessels to regional changes in load or/and tissue demands is surveyed with respect to its importance for cardiovascular function in normotension as well as in physiological (giraffes) and pathophysiological (e.g. human and rat primary hypertension) variants of high pressure states. 2. At the local level it implies an entirely appropriate adjustment of cardiovascular geometric design according to principles inherent in the LaPlace and Poiseuille laws. However, when generalized to all systemic circuits, as in primary hypertension, it invites to a potentially dangerous positive feedback interaction with even ordinary functional pressor influences. 3. It is further emphasized how resistance vessels, besides the obvious influence of changes in: (i) vascular smooth muscle activity, are greatly affected also by changes of their (ii) geometric design, (iii) wall distensibility, and (iv) transmural pressure, how each of these four parameters can be independently altered and how they interact. Genetic reinforcements and various trophic influences may facilitate the extent and rate of 'structural upward resetting' in primary hypertension, and this resetting also encompasses the barostat mechanisms. 4. Against such a background it is, in fact, from a physiological point of view, more difficult to explain how 85-90% of the population manage to maintain lifelong normotension than to explain why hypertension gradually afflicts the remaining 10-15%. It points to the presence of potentially powerful and durable, negative feedback that are still poorly understood (e.g. Muirhead's renomedullary depressor system).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1991

Is the humoral renal antihypertensive activity of the spontaneously hypertensive rat (SHR) reset to the high blood pressure?

The kidneys have a humoral antihypertensive system, located in the renal medulla and presumably antagonizing the pro-hypertensive renin-angiotensin system. Medullipin I and II and maybe platelet activating factor (PAF), seem to be the mediators of this system, known to be activated after reversal of renovascular hypertension or when the perfusion pressure to a normotensive kidney is suddenly elevated. The present study was undertaken to investigate whether this system is functioning also in the spontaneously hypertensive rat (SHR), and if it is then reset in proportion to the increased mean arterial pressure (MAP). Isolated kidneys from spontaneously hypertensive rats and from Wistar Kyoto rats (WKY) were cross-perfused in vivo from anaesthetized intact Wistar Kyoto rat 'donors'. After 30 min of perfusion at 100 mmHg the perfusion pressure to the isolated kidneys were, for 60 min, either kept unaltered at 100 mmHg or, for the Wistar Kyoto rat kidneys, increased to 150-200 mmHg and, for the spontaneously hypertensive rat kidneys, raised to 200 or 250 mmHg. The results show that the humoral antihypertensive system is present also in spontaneously hypertensive rat kidneys, but is here reset upwards to or even beyond the elevated MAP level. Furthermore, all mean arterial pressure reductions caused by high-pressure perfusion of Wistar Kyoto and spontaneously hypertensive rat kidneys were accompanied by reductions in heart rate (HR) in the 'donors', in agreement with previous observations after reversing renal hypertension and after i.v. medullipin I injection. In fact, in spontaneously hypertensive rat kidneys, the 'incretory' depressor mechanism appears to be more markedly reset upwards than is the 'excretory' depressor mechanism inherent in pressure diuresis with consequent salt-volume elimination. In conclusion spontaneously hypertensive rats, like Wistar Kyoto rats and Wistar rats, have a humoral antihypertensive system in the kidneys, but it is reset upwards even beyond the elevated mean arterial pressure level in spontaneously hypertensive rats. The combination of a depressor response and reduced heart rate in the 'donors' renders further evidence that the medullipins are the principal, though probably not the only, humoral antihypertensive factors released from the cross-circulated kidneys.

Animals↗
PubMed1991

Myogenic responsiveness in rat hindquarter vessels during constant-flow and constant-pressure perfusion in vitro; effects of various potassium concentrations and of endothelial nitrous oxide blockade.

An in vitro constant-flow, alternatively constant-pressure, perfusion method for studying microvascular myogenic responsiveness in otherwise intact rat hindquarters was used to explore how three types of influences affect the pressure-flow induced enhancements of myogenic tone: (1) Changes of potassium concentration over the range 2-50 mmol; (2) Whether myogenic responsiveness, which is fairly weak during these conditions of high shear rates, is enhanced by blockade of endothelial prostacyclin and nitrous oxide formation; (3) Whether some of the drawbacks of the constant-flow technique, like rapid edema formation, is offset by a constant-pressure variant. The result can be summed up as follows. (1) Myogenic responsiveness is also during in vitro conditions markedly influenced by even modest potassium concentration changes around the physiological resting level, e.g. showing a fourfold difference between potassium concentrations of 2.5-4.5 mmol. It was entirely suppressed above 7-8 mmol potassium concentration but also when potassium concentration values above 20 mmol increasingly depolarize and constrict the resistance vessels. (2) While blockade of prostacyclin synthesis was without effect, suppression of endothelial nitrous oxide production could increase myogenic responsiveness up to fourfold, suggesting that shear-stress dependent release of this agent serves to suppress myogenic activity. These effects were, however, quite variable suggesting that also other endothelial inhibitory influences are involved. (3) The constant-pressure variant reduces some of the methodological drawbacks, particularly the oedema formation which can be further reduced by increasing perfusate colloid osmotic pressure. However, interferences by the mentioned, partly unknown endothelial mechanisms still tend to suppress myogenic responsiveness to a varying extent, which hampers quantitative analyses particularly of other inhibitory influences.

Animals↗
PubMed1991

Blood pressure and neurogenic adaptations to reduced dietary sodium in the SHR model of hypertension.

Sodium (Na) balance is maintained by a complex set of genetic, hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. This research focused on the role of a reduction in dietary Na on cardiovascular and neuroeffector function in normotensive (WKY) and spontaneously hypertensive rats (SHR) raised from 5-20 weeks on a control Na diet (12 mmol per 100 g food) or various low Na diets (0.5-2 mmol per 100 g food). For comparison purposes, high Na (140 mmol per 100 g food) results are reported. With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% in SHRs but not in WKYs. Body weights, blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both SHR and WKY low Na groups were abnormally sensitive to blood loss and showed attenuated pressor responses, mediated by the sympathetic nervous system, to both acute and chronic stress situations. Low Na treatment significantly attenuated the pressor response during stress, which was primarily due to reduction in noradrenergic transmitter release. In spite of depressed function during restriction of dietary Na, compensatory responses were adequate to maintain homeostasis, but the neurohumoral compensatory reserve was thereby markedly curtailed. The data suggest that risks are associated with a reduced intake of dietary Na. These findings imply that the "hygienic" Na intake in man should be carefully experimentally defined before generalized measures are taken to reduce dietary Na in society.

Animals↗
PubMed1990

[Central nervous system control for maximal alertness in danger].

A survey is given of the various "emotional" neuro-hormonal response patterns, organised at the limbic-hypothalamic level of the brain and specialised in dealing with the multiplicity of challenging environmental stimuli that all organisms, including man, have to cope with. Typically they involve all three efferent links of body control--i e, the somatomotor system, governing behaviour, the visceromotor (autonomic nervous) system, adjusting inner organs to suit behavioural response, and the hormonal system, adjusting metabolism, nutritional depots and water-electrolyte balance, again to provide optimal support for behavioural response. Special emphasis is put on the visceromotor and hormonal adjustment of the cardiovascular system, affecting blood pressure, cardiac output and blood flow distribution, particularly in stressful situations, where such responses as the "defence reaction", the "defeat reaction" and the "playing-dead reaction", are virtually the same in all species. It is discussed how in humans such age-old response patterns are also elicited by a variety of artificial or symbolic challenges typical of hectic modern society; and how, if provoked too often or too long, they may constitute crucial determinants of such serious cardiovascular disorders as hypertension and atherosclerosis. In this context, the defence and defeat reactions would seem to be particularly relevant, and the importance is stressed of animal studies of such complex systemic adjustments, for the understanding and hence future prevention of certain particularly serious disorders common in modern society.

Animals↗
PubMed1990

Risks associated with dietary sodium reduction in the spontaneous hypertensive rat model of hypertension.

Sodium balance is maintained by a complex set up of hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. The focus of the following research was on the cardiovascular and neuroeffector effects of dietary Na reduction primarily in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) raised from 4 to 15 weeks on a control Na diet (CNa: 12 mmol per 100 g food) or various low Na diets (LNa: 0.5 to 3 mmol per 100 g food). With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% and raised resting heart rate (20%) in SHRs but not WKYs. Blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both LNa strains were abnormally sensitive to blood loss and showed attenuated pressor responses to both acute and chronic stress situations. Cardiac function was not altered by LNa treatment in either rat strain although structural compensations occurred. LNa treatment significantly attenuated the pressor reduction in mesenteric blood flow during stress which was primarily due to reduction in noradrenergic transmitter release and not due to altered receptor sensitivity, density, or Na/K ATPase activity. Compensatory sympathetic activity was increased as was sodium conservation through humoral mechanisms which maintained homeostasis. However, further neurohumoral compensation was markedly reduced. The data suggests that the hygienic sodium intake in humans should be experimentally defined before generalized measures are taken to reduced dietary sodium use throughout society.

Adrenergic Fibers↗
PubMed1990

"Structural factor" in primary and secondary hypertension.

The history of research on the "structural factor" in primary hypertension is briefly reviewed, and the gradual realization of its important influence on the hemodynamics of hypertension is outlined, as seen from a "personal angle." Experiences from previous studies of normal vascular function in animals were decisive for our first hemodynamic demonstration concerning the "structural upward resetting" of the systemic resistance vessels in human primary hypertension. Subsequent quantitative studies in rats with primary and secondary hypertension complemented these studies, confirming that the critical structural changes are a rapid increase in precapillary resistance at full dilatation associated with an increase in wall/lumen ratio due mainly to media hypertrophy and occurring in both primary and renal hypertension. Analyses were also performed concerning cardiac, barostat, and venous structural resettings, which are briefly mentioned. In our first studies of human primary hypertension, we suggested that the structural factor might itself be genetically reinforced, and increasing evidence in favor of this view is now accumulating. It is further discussed how antihypertensive therapy should be directed primarily against the structural upward resetting, as dependent on the local pressure and "trophic" influences, and some of our results in rat models are outlined. Finally, as the structural factor at the systemic resistance level also invites positive feedback interactions with functional "pressor" influences, it is, in a way, more difficult to explain why 85-90% of people remain normotensive than how hypertension gradually develops in 10-15% of people. This points to some powerful and durable negative feedbacks, which are still poorly understood, because most so far known barostats are readily reset upward in hypertension. It is here that the Muirhead renomedullary depressor system, and perhaps also the unmyelinated baroreceptor-volume receptor afferents, may be of particular importance.

Adaptation, Physiological↗