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Abstract

Purpose

We aimed to critically review the available information on the potential contribution of excessive kallikrein-kinin systems (KKSs) activation to severe respiratory inflammation in SARS-CoV-2 infection, and the likely consequence of ACE inhibition in seriously affected patients.

Methods

The literature related to the above topic was reviewed including papers that analysed the connections, actions, interactions, consequences and occasionally suggestions for rational interventions.

Results/Conclusion

Severe broncho-alveolar inflammation seems to be caused, at least in part, by upregulation of the KKS that increases plasma and/or local tissue concentrations of bradykinin (BK) in patients with COVID-19 infection. Besides KKS activation, suppression of ACE activity results in decreased bradykinin degradation, and these changes in concert can lead to excessive BK B1 and B2 receptor (BKB1R/BKB2R) activation. Aminopeptidase P (APP), and carboxypeptidase N also degrade bradykinin, but their protein expression and activity are unclear in COVID-19 infection. On the other hand, ACE2 expression is upregulated in patients with COVID-19 infection, so ACE2 activity is unlikely to be decreased despite blockade of part of ACE2 by the virus for entry into the cells. ACE2 cleaves lys-des-arginine9BK and arg-des-arginine9BK, the active metabolites of bradykinin, which stimulate the BKB1R receptor. Stimulation of BKB1R/BKB2R can exacerbate the pulmonary inflammatory response by causing vascular leakage and edema, vasodilation, smooth muscle spasm and stimulation of pain afferent nerves. Despite all uncertainties, it seems rational to treat comorbid COVID patients with serious respiratory distress syndrome with ARBs instead of high-dose ACE inhibitor (ACEi) that will further decrease bradykinin degradation and enhance BKB1R/BKB2R activation, but ACEi may not be contraindicated in patients with mild pulmonary symptoms.

Open access

Progressive loss of muscle mass and strength is a physiological consequence of aging, and without interventions, it usually deteriorates into sarcopenia. In this study, the hypothesis that combined special nutritional–physiotherapeutical intervention to prevent or reverse this biological deterioration in elderly people was tested. The effects of the regular resistance muscle training (PT, n = 17) alone and the combined exercise + special nutrition therapy containing whey protein and vitamin D (PT + NT, n = 17) were monitored for 3 months in 34 elderly patients (12 men and 22 women; mean age: 66.47 years) randomly distributed into two groups at a long-term care facility. Physical exercise alone did not result in significant improvement in skeletal muscle mass or strength, whereas combined intervention significantly increased the muscle strength (22.51 ± 2.35 vs. 24.54 ± 2.65, x ¯  ± SEM, kg, p = 0.027). When therapeutic responses to the intervention were compared, a significant advantage of PT + NT over PT was found. The same trend was found when the non-significant post-therapeutic alterations (χ2 test) of the distribution of normal vs. pre-sarcopenic + sarcopenic conditions within the two groups were compared. Combined intervention (PT + NT) is necessary for the efficient protection of the musculature in the high-risk elderly patients.

Restricted access
Acta Physiologica Hungarica
Authors:
M. Matrai
,
B. Szekacs
,
M. Mericli
,
G. Nadasy
,
M. Szekeres
,
F. Banhidy
,
G. Bekesi
,
E. Monos
, and
Szabolcs Várbíró

Hypertension causes small vessel remodeling, vasomotor alterations. We investigated diameter, tone and mechanics of intramural small coronaries of female rats that received chronic angiotensin treatment to induce hypertension.Angiotensin II infusion (AII, 100 ng/bwkg/min, sc.) was used to establish hypertension in 10 female rats. Other 10 rats served as controls. Following 4 weeks of treatment, side branches of the left anterior descendant coronary (diameter∼200 μm) were isolated, cannulated and pressure-diameter curves were registered between 2–90 mmHg. Changes in vessel diameter were measured in Krebs solution, in the presence of thromboxane A2 receptor agonist (U46619, 10−6M), bradykinin (BK, 10−6M), and finally at complete relaxation (in Ca2+-free solution).Chronic AII treatment raised the mean arterial pressure (130±5 mmHg vs. 96±2 mmHg, average ±SEM) significantly. Wall thickness of the AII group was significantly greater (40.2±4.2 μm vs. 31.4±2.7 μm at 50 mmHg in Ca2+-free solution), but cross-section of the vessel wall did not differ. Tangentional wall stress and elastic modulus decreased significantly in hypertensive animals. Constrictions in the presence of U46619 were greater in the AII group (24.4± 5.6% vs. 14.5±3.3% at 50 mmHg).In hypertension, intramural small coronaries showed inward eutrophic remodeling, as a morphological adaptation following AII treatment enhanced thromboxane A2 — induced tone.

Restricted access
Acta Physiologica Hungarica
Authors:
J. Stark
,
Zs Tulassay
,
G. Lengyel
,
D. Szombath
,
B. Székács
,
I. Ádler
,
I. Marczell
,
P. Nagy-Répas
,
E. Dinya
,
K. Rácz
,
G. Békési
, and
Iván Horváth

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