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Biomedical subjects

B Folkow

Publications and source records attributed to B Folkow.

188 records · Page 11Linked to original sources
PubMedDate not supplied

Measurements of plasma norepinephrine concentrations in human primary hypertension. A word of caution on their applicability for assessing neurogenic contributions.

The relationship between plasma levels of norepinephrine (NE) and sympathetic neural activity is discussed with special reference to human primary hypertension. Since sympathetic discharge is differentiated, neural activity to a given target organ will contribute variably to plasma NE levels in different situations. Hemodynamically, early primary hypertension is often characterized by a mild defense reaction-like pattern with signs of increased sympathetic activity to the heart and vasoconstriction in the renal and splanchnic vascular beds. Although important hemodynamically, these organs seem to be of less importance as contributors to peripheral plasma NE levels. In contrast, muscle sympathetic activity and muscle vascular resistance is unchanged or reduced. Since this organ mass contributes importantly to plasma NE levels, especially in peripheral venous blood, it is not surprising that most patients with primary hypertension have normal NE levels. It is concluded that NE concentrations in forearm or mixed venous blood are unreliable indicators of sympathetic neural contributions to essential hypertension, tending to underestimate this element, and that regional measurements of NE overflow are needed for a reliable analysis.

Hemodynamics↗
PubMedDate not supplied

Structural factors: the vascular wall. Consequences of treatment.

Like all tissues, blood vessels readily adapt their structure upon sustained functional changes. For example, pressure increases soon induce a largely proportional wall (w) thickening, where arteries, veins, and true resistance vessels respond alike. The latter also show a modest structural narrowing of average inner radius (ri), where the increased w/ri ratio results in a geometrically based vascular hyperreactivity. In primary hypertension, this type of precapillary resistance vessel adaptation implies an important "upward structural autoregulation" of systemic resistance, which is thereby kept increased also when vascular smooth muscle activity is entirely normal. Further, the systemic vascular hyperreactivity introduces a positive feedback interaction with functional pressor influences. By this mechanism, even marginal increases in "functional drive" may, if only sustained, steadily enhance the structural w/ri increase until it dominates hemodynamics. Similar alterations of the renal preglomerular vessels cause an early upward resetting of the renal barostat function, while wall thickening of large arteries helps to reset the baroreflexes. Also, the capacitance vessels show some structural adaptation that reduces venous compliance and contributes to blood volume centralization. Due to this overall structural resetting of hypertensive cardiovascular systems, the pharmacological problem of normalizing blood pressure is not one of merely damping an increased vascular smooth muscle activity. The task is more formidable, because effector cell activity must be kept even subnormal, despite counterregulatory mechanisms. These mechanisms almost all have been redesigned to maintain the high pressure state, with the long-range goal that true regression toward normality should ultimately ensue.

Aging↗
PubMedDate not supplied

Antihypertensive polar and neutral renopapillary lipids. Which is a hormone?

Two antihypertensive lipids can be derived from the renal papilla, the antihypertensive polar (APRL) and the antihypertensive neutral (ANRL) renomedullary lipid. The renal venous effluent of the unclipped kidney contains both ANRL and APRL. This effluent lowers the arterial pressure (AP) of the normal rat when infused i.v. As it lowers the AP the heart rate (HR) and sympathetic nerve activity (SNA) are depressed. ANRL infused i.v. also lowers HR and SNA as it depresses the AP. Conversely, APRL elevates HR and SNA as it lowers the AP. Thus, of the two lipids in the renal venous effluent after unclipping, ANRL appears to be dominant. APRL, however, in the renal venous effluent could potentiate the action of ANRL. The net effect of these observations is to support the view that ANRL is an antihypertensive hormone liberated by the kidney after unclipping. The renomedullary interstitial cells (RIC) degranulate after unclipping. ANRL can be derived from these cells. Thus, the RIC, cells known to exert an endocrine-type antihypertensive function, may well be the source of ANRL in the renal venous effluent after unclipping. The hormonal action of ANRL appears as a major cause of the lowering of the AP after unclipping. It is not known what factors modulate the RIC endocrine system. There is a suggestion that angiotensin may be one of these factors based on the ineffectiveness of these cells toward retarding hypertension when the circulating plasma angiotensin level is high, and their effectiveness when the circulating plasma angiotensin level is low.

Angiotensins↗
PubMedDate not supplied

Brief historical background and principal nature of process.

After a brief outline of the historical background, the biological principle of structural tissue adaptation to alterations in load is discussed with special reference to the cardiovascular system. It is stressed that adaptive changes of cardiac and vascular design to local load are rapid, precise, and, on the local level, highly appropriate. However, in hypertension, when they affect the entire systemic resistance section (structural autoregulation), as well as some major "barostats," an upward structural resetting of the entire pressure equilibrium occurs. Further, by way of the consequent vascular resistance vessel hyperreactivity, a positive feedback interaction is established with functional pressure effects and thus tends to further escalate the pressure rise. For these reasons the "normal" structural factor becomes of key importance for the initiation, maintenance, and gradual aggravation of chronic high pressure states.

Adaptation, Physiological↗
PubMedDate not supplied

Consequences of structural renovascular changes for renal barostat function.

During maximal vasodilatation the renal vascular beds of normotensive control rats (NCR), uninephrectomized NCR (U-NCR), spontaneously hypertensive rats (SHR), and two-kidney, one clip renal hypertensive rats (RHR) have been compared concerning glomerular filtration capacity, total renovascular resistance, and the relationship between perfusion pressure and glomerular filtration rate (GFR). The GFR reflects the important ratio between the preglomerular and postglomerular resistances that is a major determinant of GFR, and during maximal vasodilatation it shows whether, and how, this ratio is altered by differentiated renovascular structural adaptation. In SHR hypertension this ratio soon becomes increased to match the pressure rise as a result of structural changes, which implies a most efficient upward resetting of the renal barostat function. Later the postglomerular resistance is also raised in SHR as a result of structural changes. This adaptation presumably occurs to offset the gradual deterioration in glomerular filtration capacity. In the clipped, "low-pressure" RHR kidney, only the preglomerular resistance is reduced, a local adaptation tending to offset the effect of the artificial inflow hindrance on GFR as a result of structural changes. In the "pressure-exposed" RHR kidney the preglomerular and postglomerular resistances are both equally increased, again as a result of structural changes. In this situation, therefore, resetting of the renal barostat function occurs less efficiently than in SHR. This may explain the observation that arterial pressure readily normalizes in RHR on declipping. The hypertrophic U-NCR kidney shows a proportional and uniform outgrowth of the renovascular bed, thus without altering the pre-postglomerular resistance ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Early versus late onset of therapy. Experiences from animal studies.

Established primary hypertension is characterized by an "upward structural resetting," that encompasses all pressure-exposed cardiovascular sections. This also affects several of the dominating barostat mechanisms, such as those based on the cardiovascular baroreceptors and volume receptors and on the renal excretory function. One major long-term goal in antihypertensive treatment, therefore, is to achieve reversal and, if possible, normalization of this structural resetting, the more so because such reversal would also interrupt the positive feedback interaction with functional excitatory mechanisms. It is, however, very difficult to analyze precisely the rate and extent of structural cardiovascular reversal in humans, and also whether some antihypertensive drugs are in these respects more efficient than others. In this respect, model therapy studies in rat primary hypertension offer several advantages, thanks to the greatly compressed time scale, uniform material, and easily controlled conditions. This facilitates the elucidation of such important problems as the relative merits of early versus late treatment and optimal duration and intensity of treatment, as well as which drug actions are most efficient in normalizing cardiovascular design. The relatively few rat model studies of structural cardiovascular reversal so far performed are outlined briefly. It is concluded that extended studies along these lines would be of great value in clarifying some general principles of antihypertensive treatment that are also likely to be relevant to primary hypertension in humans.

Animals↗