Biomedical subjects

N Sjöblom

Publications and source records attributed to N Sjöblom.

8 recordsLinked to original sources

PubMed1987

Post-tetanic potentiation of the vascular neurogenic response in rats.

We have previously shown that, at least at frequencies of 4 Hz and above, a previous stimulation of the intramural vasoconstrictor nerves facilitates the subsequent response so that even maximal contractions can develop during periods of stimulation as short as a few seconds. In the present study the facilitating effect of a continuous nerve stimulation was quantitatively tested on 'single-twitch' responses to individual nerve impulses. Small arteries and veins (150-500 micron diameter) from rats were mounted in a myograph at known wall tension, and the intramural nerves were activated at frequencies between 0.1 and 32 Hz. After a period of continuous stimulation the single-twitch responses could be amplified 10-20 times, depending on frequency and duration of the continuous stimulation. No such amplification was observed after application of exogenous noradrenaline. The results therefore reflect a prejunctional frequency-dependent potentiating mechanism which can strongly reinforce sympathetic neuroeffector control. Furthermore, combined with previous data concerning adrenergic transmitter release, the present results seem to be more compatible with the view that the quantum of transmitter released from each varicosity upon activation is less than an entire granule.

Animals↗

PubMed1985

The influence of the sympathetic impulse pattern on contractile responses of rat mesenteric arteries and veins.

Contractile responses to electrical field stimulation of excised small mesenteric arteries and veins of the rat were compared when stimuli were delivered in irregular bursts or at regular intervals. Spontaneously occurring skin vasoconstrictor impulses in a few-unit median nerve recording in man were stored on tape and used to trigger a stimulator. Two irregular stimulation sequences at average frequencies of 1.6 and 1.8 Hz, respectively, were used. In the arteries, average contractile responses were significantly greater at an irregular than at an even stimulation frequency, but in the veins, similar degrees of contraction were obtained with the two modes of stimulation. The frequency-response relationships to continuous regular stimulation showed the artery to respond less than the vein at low frequencies. This apparently explains the differences in behaviour between the vessels to irregular stimulation. The results show that not only the number of impulses, but also their pattern of occurrence, may influence the degree of vasoconstriction. Thus, the normal irregular sympathetic discharge pattern in itself has a bearing on the physiology of neuro-effector control mechanisms.

Animals↗

PubMed1985

Interaction between prejunctional alpha 2-receptors and neuronal transmitter reuptake in small mesenteric arteries from the rat.

The role of the prejunctional alpha 2-receptors for the response to vaso-constrictor nerve stimulation has been examined before and after inhibition of neuronal transmitter reuptake in mesenteric resistance vessels from the rat. Small arteries (diameter about 200 micron) feeding the jejunum were mounted in a myograph for recording of their isometric wall tension during transmural field stimulation of the intramural nerves. Blockade of prejunctional alpha 2-receptors with 0.01 microM idazoxan (RX 781094) caused a marginal potentiation of the neurogenic response when neuronal reuptake was left intact. Also, inhibition of reuptake alone with 3 microM cocaine had little effect on the response. However, when both alpha 2-receptors and reuptake had been inhibited, a strong enhancement of the neurogenic vasoconstriction was observed. Similar findings were made when yohimbine and LU 3-010 instead were used for alpha 2-blockade and reuptake inhibition, respectively. The results thus indicate that in these resistance arteries the effector response is normally influenced by the combined activity of alpha 2-receptors and uptake, and that failure of one mechanism increases the activity of the other, so as to maintain a largely constant effector response.

Adrenergic alpha-Agonists↗

PubMed1985

Distension-dependent changes in noradrenaline sensitivity in small arteries from the rat.

The effects of distension on the sensitivity to noradrenaline and potassium were assessed in ring preparations of 200 micron branches from the superior mesenteric artery of the rat. In response to noradrenaline, maximal tension development occurred at smaller luminal diameters than with potassium activation. The sensitivity to noradrenaline increased with increasing distension whereas potassium sensitivity remained largely unchanged. A distension-dependent increase in noradrenaline sensitivity was observed also in vessels depolarized with high-potassium solution. The role of the distension-dependent sensitivity to noradrenaline for isotonic contractions was also studied. Upon activation with applied noradrenaline, submaximal isotonic responses were somewhat smaller than isometric responses at the same dose. This may be ascribed to a reduction in sensitivity during the isotonic contraction. Upon neurogenic activation, no difference between isotonic and isometric responses was found. The results show that distension increases noradrenaline sensitivity in resistance vessels in vitro, but that the consequences for their function as neuroeffectors may be small.

Animals↗

PubMed1985

Neurogenic responses in resistance vessels: roles of alpha 1- and alpha 2-adrenoceptors, transmitter reuptake, ouabain, and plasma factors.

Experiments on the vasoconstrictor fiber control of isolated spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) resistance vessels, which is throughout more efficient in SHR, suggest that the presynaptic alpha 2-negative feedback mechanism and the reuptake pump are largely complementary in adjusting the effective transmitter concentrations in these narrow junctions, and first when both are blocked a marked leftward displacement of the nervous frequency-response curve ensues. Also, ouabain causes a marked leftward displacement of the frequency response curve in a way which suggests a considerable increase of transmitter release/impulse. Finally, normal rat plasma contains agent(s) which, even in very low concentrations, seems to cause a strong ouabain-like effect on the neurogenic responses. However, these various interferences with the neurogenic vascular effects influence SHR and WKY to largely equal extents, implying that the more efficient nervous control in SHR vessels is not merely due to an altered balance of the ordinary local mechanisms that influence the adrenergic transmitter release.

Animals↗

PubMed1984

How do changes in diameter at the precapillary level affect cardiovascular function?

A survey is given of the various high-pressure precapillary vascular sections and of how they affect local and overall cardiovascular functions, with special emphasis put on the important "precapillary resistance vessels." The complex interactions between hemodynamic effects dependent on (a) vessel design, (b) transmural pressure, (c) "passive" wall distensibility, and (d) "active" smooth muscle responses are outlined in principle and experimentally illustrated with respect to systemic resistance control. Particular attention is devoted to the influence of the sympathetic vasoconstrictor fibers on precapillary vascular functions, concerning aspects such as speed, precision, range, and differentiation of the neurogenic effects, because these fibers represent the most powerful and widespread of the vascular control mechanisms involved in cardiovascular homeostasis. How these fibers in well-innervated vascular circuits can command up to the maximum contractile capacity of both the precapillary resistance and postcapillary capacitance vessels is illustrated, as well as the way in which these sets of vessels respond to even single nerve impulses with twitchlike, rapid contractions.

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↗

PubMed1984

Extent of alpha 2-receptor-mediated autoinhibition of vasoconstrictor nerve responses in mesenteric resistance vessels from normotensive and hypertensive rats.

The authors have previously shown that vasoconstrictor nerve responses of mesenteric small arteries from spontaneously hypertensive rats (SHR) are increased compared with normotensive rats. In this paper, whether this is due to differences in the degree of negative feedback of the transmitter on its own release is investigated. Small (i.d. 200 microns) arteries from the mesenteric arcades of SHR and normotensive control rats (NCR) were mounted in a Mulvany-Halpern myograph. In both SHR and NCR, nerve stimulation and applied noradrenaline elicited maximal contractions of similar magnitude, although SHR vessels were somewhat stronger and more responsive to nerve stimulation. Blocking alpha 2-receptors with 10 nM RX 781094 reduced the frequency for half-maximal activation to 84% and 80%, respectively, but did not eliminate the difference between the strains. Presynaptic alpha 2-receptors thus do not seem to cause the enhanced vasoconstrictor responses in SHR vessels.

Adrenergic alpha-Antagonists↗