Læknablaðið - 15.11.1996, Síða 51

LÆKNABLAÐIÐ 1996; 82
795
Nýr doktor í læknisfræði
Þann 14. maí síðastliðinn varði Hrafnhildur
Soffía Guðbjörnsdóttir doktorsritgerð við Há-
skólann í Gautaborg. Ritgerðin nefnist Studies
on the relationships between insulin resistance,
sympathetic nerve activity and hypertension.
Ágrip úr ritgerðinni fer hér á eftir.
Primary hypertension is associated with in-
sulin resistance and compensatory hyperinsuli-
nemia. The sympathoexcitatory effect of in-
sulin has been suggested to constitute a patho-
physiological link between insulin resistance/
hyperinsulinemia and primary hypertension.
The aim of the present study was to elucidate
the relationships between insulin resistance/
hyperinsulinemia, sympathetic neuro-humoral
activity and the arterial blood pressure level.
In obese, middle-aged hypertensive men it
was found that insulin does not elicit an acute
hypertensive effect, even in severely insulin-
resistant subjects lacking the normal vasodila-
tory response to insulin. Sympathetic re-
sponses to acute hyperinsulinemia were found
to be differentiated, with excitation predom-
inantly of nerves supplying the muscle vascular
bed (MSA), leaving total body and renal nor-
epinephrine spillover unchanged. However,
the studies also confirm a relationship between
fasting plasma insulin levels and blood pres-
sure, although a clear insulin resistance was
not present in all hypertensive subjects. A
weak correlation between fasting insulin levels
and MSA was found in hypertensive subjects,
but it is unlikely that the increased MSA con-
stitutes the underlying mechanism for hyper-
tension since their resting MSA levels did not
differ significantly from a BMI- and age-
matched normotensive control group.
Antihyperglycemic agents that increase in-
sulin sensitivity, e.g. metformin, have also
been used to test the hypothesis that insulin
resistance /hyperinsulinemia contributes to in-
creases in arterial pressure. In the present
studies, metformin had no significant effects
on insulin sensitivity or blood pressure in in-
sulin-resistant normoglycemic hypertensive
men. It is suggested that the vascular effects of
metformin found in NIDDM subjects could be
related to the metabolic effects of metformin
treatment rather than being direct effects of
metformin. It has been claimed that antihyper-
tensive treatment with B-adrenergic blocking
agents decreases insulin sensitivity. In con-
trast, we found that metoprolol did not signif-
icantly affect insulin sensitivity but seems to
alter the distribution or degradation of insulin
hypertensive subjects undergoing an insulin
clamp.
In conclusion, the studies confirm the lack of
hypertensive effect of an acute hyperinsuline-
mia, despite a marked excitation of muscle
sympathetic nerve activity. This finding may
reflect a differentiated sympatho-excitation,
rather than being explained by an opposing
vasodilatory effect of insulin. The present
studies in subjects with established hyperten-
sion do not give evidence for a causal relation-
ship between the insulin-induced increase in
MSA and hypertension. Longitudinal studies
in insulin-resistent normotensive subjects will
be necessary to elucidate the relationship be-
tween chronic hyperinsulinemia and establish-
ed hypertension.