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Biomedical subjects

B Folkow

Publications and source records attributed to B Folkow.

At least 91 records · Page 5Linked to original sources
PubMed1984

Age- and pressure-dependent changes of systemic resistance vessels concerning the relationships between geometric design, wall distensibility, vascular reactivity and smooth muscle sensitivity.

The resistance vascular function in normotension, and its alterations in primary hypertension and ordinary aging, was analysed concerning the interactions between geometric vascular design, wall distensibility, transmural pressure and smooth muscle activity. Paired hindquarter perfusions were used, comparing hemodynamic resistance characteristics in young, adult and old normotensive (WKY) and spontaneously hypertensive rats (SHR). From the experimental data pressure-resistance diagrams were constructed, which quantitatively interrelate the four factors in all SHR-WKY groups. The diagrams show, over a wide pressure range, how altered smooth muscle activity as well as structural adaptation affect resistance vessel distensibility; likewise how distensibility considerably interferes with "active" resistance adjustments. They also show how markedly the range of active resistance responses during ordinary constant-pressure perfusion is affected whenever pressure is reset to new levels. Finally, the diagrams illustrate the fundamental hemodynamic difference between hypertensive and normotensive resistance vessels, mainly because of factors 1 and 2, which render the hypertensive vessels stronger, stiffer and hyperreactive. Thereby they are capable of a widened response range despite the higher pressure level, which is further accentuated on acute pressure normalization. In contrast, ordinary aging alters resistance vascular behaviour only little, smooth muscle contractility and sensitivity remaining almost unchanged. However, vascular reactivity is moderately enhanced at lower pressures, presumably a geometric consequence of age-dependent, intimal-interstitial endowment.

Aging↗
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↗
PubMed1984

Effects of low and high Na diets on cardiovascular dynamics in normotensive and hypertensive rats: neuroeffector characteristics of the resistance vessels.

The aim of the study reported was to explore differences in neuro-effector characteristics of the resistance vessels from normotensive and hypertensive rats (WKY and SHR), which from five to twelve weeks of age had been exposed to either low-sodium (0.5 mM/100 g food), control-sodium (5 mM/100 g) or high-sodium (50 mM/100 g) diet. Isolated small mesenteric arteries (diameter 150-200 microM) were mounted in a two-vessel Mulvany-Halpern myograph. Noradrenaline sensitivity was similar in all arteries. Frequency-response curves of SHR arteries were steeper than in WKY. In both strains low-sodium curves were displaced to higher frequencies with little difference between control and high-sodium curves. Inhibition of the Na-K-ATPase with ouabain enhanced neurogenic responses more than noradrenaline responses, but to similar extents in all sodium groups. The results suggest that chronic low-sodium diet substantially reduces the total adrenergic transmitter release per impulse.

Animals↗
PubMed1983

'Structural autoregulation'--the local adaptation of vascular beds to chronic changes in pressure.

Blood vessels readily adapt their design in response to sustained functional changes. If pressure (P) increases, the resulting thickening of the walls (w) of the resistance vessels, associated with a reduction in average inner radius (ri), keeps wall tension per unit wall layer (T) constant, because the increased w/ri ratio largely balances the raised pressure (Laplace's law: T = P X ri/w). The opposite occurs when there are sustained reductions in pressure. This locally elicited, mainly precapillary structural adaptation is a long-range equivalent to precapillary functional autoregulation and deserves to be called structural autoregulation. In primary hypertension there is an early 'structural resetting' of the systemic precapillary resistance, due to narrowing of ri and to vascular hyperreactivity ensuing from the increase in w/ri. These structural changes imply an increased resistance to flow at normal levels of vascular smooth muscle activity. Furthermore, even mild functional pressor influences will, if sustained, by a positive feedback interaction with the initially mild vascular hyperreactivity gradually accentuate the structural increase in w/ri. Marked rises in pressure may ensue from this interaction, implying that it is a major causative element in primary hypertension. As the renal preglomerular resistance vessels are similarly structurally autoregulated, this implies an early largely parallel resetting of the important renal 'long-term barostat function'. Further, as the walls of large arteries get thicker and stiffer, this helps to reset the baroreceptors. Finally, as the venous capacitance vessels adapt in a similar way the slight rise in average venous pressure in primary hypertension will reduce venous compliance, which helps to 'centralize' the usually slightly reduced blood volume.

Adaptation, Physiological↗
PubMed1983

Neurotrophic effects on the vascular bed.

After defining truly "neurotrophic" influences, and giving examples from the many studies of such influences on the somatomotor system, current research concerning sympathetic neurotrophic effects on the vascular bed is discussed. Tissue-culture studies have made it clear that, particularly in early growth phases, local trophic influences are quite important and interdependent between adrenergic neurons and vascular smooth muscle cells. Most experiments aimed at illustrating neurotrophic effects on vascular beds in vivo, however, seem to suggest the dominance of long-term adaptation processes inherent in the effector cells themselves which, particularly on sustained extrinsic activation however achieved, become increasingly mobilised. This is not to dispute the fact that truly neurotrophic influences seem to be superimposed, facilitating and modulating these essentially intrinsic mechanisms for long-term effector cell adaptation, but their relative importance is difficult to judge.

Animals↗
PubMed1983

Age-dependent alterations in the structurally determined vascular resistance, pre- to postglomerular resistance ratio and glomerular filtration capacity in kidneys, as studied in aging normotensive rats and spontaneously hypertensive rats.

Maximally dilated renal vascular beds of 13-month-old NCR and SHR were compared to explore how aging respectively longstanding primary hypertension structurally alters total renal resistance, pre/postglomerular resistance ratio and maximal glomerular filtration capacity, as measured per unit kidney weight. According to comparisons of 1.5- and 3.5-month-old NCR and SHR (Folkow et al. 1977), a structurally increased pre/postglomerular resistance ratio rapidly resets the renal "longterm barostat function" in SHR to match the 30-40% pressure rise, thereby increasing total renal resistance 15-20%, while filtration capacity is unaltered so far. In NCR aging to 13 months hardly alters arterial pressure, but increases total renal resistance 10-15%, mainly affecting postglomerular vessels, while filtration capacity is reduced 25%. 13-month-old SHR show an additional 15% pressure rise and--relative to agematched NCR--a further 35% reduction of filtration capacity with a 30-35% increase of total renal resistance, which mainly affects the postglomerular vessels as the resistance ratio is now barely above that in NCR. Thus, advancing SHR hypertension seems to start a renal vicious circle, because accentuated reductions of filtration capacity are parallelled by structural postglomerular resistance increases apparently to maintain GFR by raised filtration pressure which, however, accelerates glomerular deterioration.

Aging↗
PubMed1983

"Structural autoregulation" of blood flow and GFR in the two renal vascular beds from two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uni-nephrectomized and intact normotensive rats.

Both kidneys from two-kidney, one-clip renal hypertensive rats (RHR) and the hypertrophied kidney of uni-nephrectomized rats (UNR) were investigated during artificial perfusion with 2% Dextran solution and kerosene at maximal vasodilatation, and studied with respect to organ weight, vascular resistance, preglomerular/postglomerular resistance ratio and glomerular filtration capacity. Paired perfusions were throughout used, isolated kidneys from age-matched normotensive rats serving as controls. The untouched, "high-pressure" RHR kidney had increased 40% in weight/100 g b.w. while its vascular resistance at maximal dilatation had increased almost 60%/g organ weight. Glomerular filtration capacity and preglomerular/postglomerular resistance ratio remained, however, largely unchanged. The clipped "low-pressure", RHR kidney was reduced 40% in weight and 45% in renal vascular resistance/g organ weight. It also showed a reduced pre/postglomerular resistance ratio and some reduction of filtration capacity. The remaining hypertrophied kidney in UNR had increased 40% in weight, while its vascular resistance and filtration capacity/g organ weight, as well as its pre/postglomerular resistance ratio were unchanged. It is concluded that the kidney in renovascular hypertension rapidly adapts structurally not only in tissue mass, but also concerning total vascular resistance and pre/postglomerular resistance ratio, so as to chronically "autoregulate" GFR to match the altered pressure situation. Likewise, after unilateral nephrectomy the remaining, normotensive kidney increases in mass, with matched increases in blood flow and glomerular filtration capacity, while total resistance/g organ weight and the pre/postglomerular resistance ratio remain at normotensive levels.

Adaptation, Physiological↗
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↗
PubMed1983

Response to slow, graded bleeding in salt-depleted rats.

The response to slow bleeding was studied in rats on low sodium intake (0.04%) versus 'ordinary' (0.4%) intake. After 12 days on the diets acute experiments were performed on paired, conscious rats. Initially the salt-depleted rats had slightly lower mean arterial pressure (121 +/- 2 versus 129 +/- 3 mmHg, n = 30 pairs, P less than 0.02). Heart rate (HR), cardiac output, plasma volume, extracellular volume and plasma renin activity (PRA) did not differ significantly, while haematocrit was slightly higher in the salt-depleted rats (46.5 +/- 0.3 versus 45.1 +/- 0.5%, P less than 0.05). The animals were then slowly bled 1 ml every 5 min until mean arterial pressure (MAP) fell and remained below 50 mmHg. The controls tolerated up to a 55 +/- 1% loss of initial blood volume, while the salt-depleted rats turned into irreversible shock already after losing 38 +/- 2% (P less than 0.001). At this stage compensatory haemodilution, HR and PRA increases were less pronounced than in the controls, suggesting that chronic sodium restriction had somehow interfered with the neurohormonal defences against accidental salt fluid losses.

Animals↗
PubMed1982

Permeability of fenestrated capillaries in the isolated pig pancreas, with effects of bradykinin and histamine, as studied by simultaneous registration of filtration and diffusion capacities.

Combining an isogravimetric technique and a colorimetric 'on-line' method (Rippe & Stage 1978), filtration capacity (CFC) and diffusion capacity (PS) were simultaneously measured in the maximally vasodilated 'fenestrated' capillary bed of isolated, artificially perfused pancreatic glands in 12 juvenile pigs. Both CFC and PS for Cr-EDTA were about 20 times greater than in the 'continuous' capillary bed of skeletal muscle. With perfusate flow rates of 250 ml/min x 100 g during isogravimetry, PS-Cr-EDTA averaged 110 +/- 10.0 (S.E.) ml/min X 100 g, and diffusion limitation occurred first at flow rates above 300 ml/min X 100 g. CFC was independent of flow rate and averaged 0.641 +/- 0.027 ml/min X 100 g X mmHg. The parallel augmentation of PS-Cr-EDTA and CFC in the fenestrated capillary bed compared with continuous ones seems to reflect both a higher number of capillaries per unit tissue and an increased number of 'small pores' per unit capillary surface, whilst the 'large pore system' appears to be similar. Following bradykinin or histamine infusion, results were similar to those for continuous capillaries (e.g. Rippe, Kamiya & Folkow 1978). Thus, without further vasodilatation CFC increased 3-fold While PS-Cr-EDTA increased only some 25%, and subsequent isoprenaline infusion reversed these effects. Previous studies on continuous capillaries indicate that histamine-type agents act by opening additional 'large pores' in the venular exchange sections (cf. Rippe & Grega (1978, Svensjö 1978), while beta-adrenergic agonists block this effect. The results further suggest that the fenestrae are not involved in these bradykinin-histamine effects, but rather function as a high-density, small pore population.

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↗