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Beta-Adrenoceptors and Beta Blockers

Discuss about the Effects of E-Adrenoceptor Antagonists on Exercise Induced Cardiovascular Changes.

Beta – adrenoceptors are binded  by beta blockers drugs which block the binding of norepinephrine and epinephrine receptors. These cause inhibition of the effects which act on the receptors. Beta blockers act as drugs which are sympatholytic. Often beta blockers bind to beta-adrenoceptors which partially activates the receptors which activates them while offering prevention of norepinephrine from binding the receptor. The partial agonists thus provide backgrounds for sympathetic activity while offering prevention of normal and enhanced sympathetic activity. The beta blockers possess aspect of intrinsic sympathomimetic activity while others produce stabilizing activity, thus producing similar activites as observed on membrane stabilization activity by sodium channels blockers.[i]

Beta blockers bind themselves to beta adrenoceptors which are located in cardiac area surrounding the nodal tissue, which conduct the system and offers contraction of myocytes. The beat has been shown to have both β1 and β2 adrenoceptors, which the common is β1 adrenoceptors. It offers binding effect on the norepinephrine which releases itself to sympathetic nerves located in adrenergic area. Beta blockers in this case offer binding protection to normal ligand β-adrenoceptors through competing itself on the binding sites.[ii]

Beta adrenoceptors are coupled by the Gs protein which offers activation of adenyl cyclase forming Camp located in the ATP which increases the Camp and thus activated the dependent protein kinase. With the general level of sympathetic tone in the heart, these beta blockers are able to lower down the sympathetic influence which offers stimulation of the heart rate, contractility, electrical conduction and relaxation. This leads to reduction in heart rate, contractility, velocity conduction and relaxation. These kinds of drugs have been shown to have an effect on the elevated levels of sympathetic activity.[iii]

With concern of cardiovascular health, beta blockers often offer little vascular effect due to the β2 adrenoceptors having small function of the modulator in the basal vascular tone. Blockage of β2 adrenoceptors is linked to smaller degree of vasoconstriction in the vascular beds.[iv]


Studies have shown that β1 and β2 adrenoceptor receptors are associated increased intensity of vascular activity, it stimulates in response to the constriction and relaxation of the arteries and veins.[v] Endothelial cells are not produced through mediation of β1 and β2 adrenoceptors, rather they play a key role in influcneing blood vessel activity, further the role played the vascular activity is key in prevention and treatment of vascular disease, thus assessing the different morphology of cardiac function is relevant in establishing effects of β1 and β2 adrenoceptors. [vi]

Effects of Beta-Adrenoceptor Antagonists on Cardiovascular Health

Beta-adrenoceptor antagonists function in cardiovascular management by lowering elevated blood pressure. Compounds such as Atenol selectively apply to Beta 1-adrenoceptor which possess intrinsic sympathomimetic activity. [vii] Pindol on the other hand has non selective ability of beta-adrenoceptor which possesses sympathomimetic activity. These study evaluates its application when used in two body states that is during rest and exercise activities, medical and therapeutic effects of both drugs is being tested. The study is a double blind using vitamin B6 as a placebo control.

This study thus seeks to examine the effects of orally administered β adrenoceptors antagonists, Atenolol and Pendolol on the blood pressure effects, heart rate and lung function during two critical phases of rest and after exercise activity.

The study experiment was submitted to the University of New South Wales, health science department for ethical approval. This experimental study employed double blind design , where subjects were blinded and utilized placebo and control usage. The subject participants involved students aged between 18-65 years of the University of New South Wales.

The materials need for this study included Perceived Exertion Scale, heart rate monitor having watch, strap and polar, blood pressure monitor, peak flow meter and a timer. The experimental phase involved two stages; pre drug and post drug . at the pre drug phase, the start the timer at 0 minutes and time adjusted to resistance level to obtain the KP level, then hold KP level at 50rpm for 2 minutes. During the last 10 seconds, recording of the heart rate, (EHR) and exertion level are undertaken. At 15 minutes recoding s of resting heart rate (RHR) is taken, while at 30 minutes, RHR, oxygen saturation, blood pressure and lung function is undertaken. Then bike exercise undertaken while the KP levels is set at 2 minutes repeat the assessment of EHR, oxygen saturation and exertion levels.

At post drug level, drug is consumed and measurements taken at 15 minutes rest, record thee RHR, oxygen saturation, blood pressure and lung function test for the participant, again the assessments are undertaken at 30 minutes , rest, 45 minutes rest, 60 minutes rest, 75 minutes rest  and 90 minutes rest post drug ingestion rest level . after 90 minutes start the bike then set at KP levels  for 2 minutes then take the assessments of HER, oxygen saturation and exertion level.

Pre drug treatment results

Time/min

Resting heart rate

beats/min

BP- dbp/sbp

mmHg

PEFR

L/min

ROS

SpO2

%

EOS

EHR

Beats/min

Fatigue

Rest

Exercise

0

82

115/76

434

98

97

399

10.6

15

87

116/75

441

97

30

86

113/74

445

97

95

114

11

Average

84

117/75

440

97

97

215

11.2

Table 1 showing the pre drug assessment of the various assessment indicators.

Study Design and Method

Key ; PEFR(Peak expiratory flow rate), ROS( rate of oxygen saturation ), EOS(Exercise oxygen saturation), HER- (Heart exercise rate)

Post drug treatment results

Time/min

SBP/DBP mmHg

Vit B6

Atenolol

Pendalol

60

117/72

113/69

106/70

90

118/70

107/67

104/65

120

115/69

108/70

101/64

Average

116/71

109/68

103/66

Table 2 showing the blood pressure assessment

Time/min

RHR beats/min

Vit B6

Atenolol

Pendalol

60

79

79.5

71

90

79

79

72

120

82

82

71

Average

80

80

71.

Table 2 : showing resting heart rate               

Time/min

PEFRL/min

Vit B6

Atenolol

Pendalol

60

475

451

415

90

460

456

450

120

480

457

451

Average

471

451

438

Table 3 showing the rate of peak expiratory rate

Time/min

ROS

SpO2%

Vit B6

Atenolol

Pendalol

60

97.6

98

97.08

90

97.3

98.16

97.03

120

97.5

97.3

97

Average

97.4

97.6

97

Table 4 showing rate of oxygen saturation

Resting heart rate

Time

Resting heart rate

beats/min

Vit B6

Atenolol

Pendalol

60

123

116

103

90

130

112

96.8

120

130

102

98.8

Average

127

110

99

Table 5 showing resting heart rate

Exercise oxygen saturation levels

Time/min

EOS

Vit B6

Atenolol

Pendalol

60

97.6

97.33

96.5

90

98

97.5

97

120

97.3

96.8

96

Average

97.5

97

96.5

Table 6 showing exercise saturation levels

Exercise fatigue levels of the assessments

Time/min

Fatigue

Exertion level

Vit B6

Atenolol

Pendalol

60

10.1

12.25

11.5        

90

10.9

12.5

11.8

120

11.3

13

12.9

Average

10.7

12.3

11.5

Table 7 showing exercise fatigue levels

The results indicate that there is elevated blood pressure with intake of the treatment. Pre drug assessments shows an average of 117/75, while on drug administration, the blood pressure was lowered significantly to 109/68 for Atenol drug and Pendalol at 103/66 beta blockers. Blood pressure ranges 90/60 or less, signifies low blood pressure, while between ranges of 90/60 to 120/80 shows ideal pressure and 140/90 and above signifies high blood pressure. The peak expiratory flow rate indicated an average of 451 L/min for Atenolol and 438 for Pednalol.  The results were comparable at the pre drug phase where there was an average of 44L/min signifying higher effect of beta blockers on lung functionality. The heart beat rate showed an average of 215 beats/min on pre drug treatment compared to 127 beats/min for the placebo, 110 beats for Atenolol drug and 99 beats/minute for pendadol drug. There was higher effect of the beta blockers on drug administration by lowering the heart beats of the sample participants.

Β-Blockers being the common drugs for lowering blood pressure has been used in hypertension management. The results in this study have showed the effect of the β-Blockers on the blood pressure. There is lowered blood pressure both systolic and diastolic signifying change effect. Its pharmacological effect acts on the intrinsic sympathomimetic activity which has adrenergic properties which block production of nitrix oxide portraying hydrophilic and lipophilic properties on blood. Combined with activity levels, it improves health outcomes through effect of cardio respiratory effects. [viii]

Peak expiratory flow rate refers to the expiration speed it signifies the rate at which there is forceful exhalation of air. It reflects airway flow and this relies heavily on the voluntary effort and muscular ability of the patient. Maximum airflow is observed during effort depends on expiratory maneuver. Peak expiratory rate on medication showed an average of 97.6% under Atenol drug, 97% under pendadol drug and at 97.4%  for Vitamin B 6. Compared to pre drug administration the average peak expiratory rate is 97% showing no significant difference.

Results

On exercise levels average resting heart rate for Atenolol and Pendadol is 110 betas/min and 99beats/min respectively compared to that of placebo which is 127 beats/min. on pre drug assessment the heart beat rate is 215 beats/min, signifying lowered levels of heart beat rate. Oxygen saturation rate level signifies an average of 97% on Atenolol drug, pendalol at 96.5% compared to placebo level at 97.5%. pre drug assessment showed an average of 97% showing no signifying difference.

Fatigue levels on exercise showed an average of 12.3 levels on Atenolol drug and a level of 11.5 on Pendalol level compared to 10.7 levels on placebo. Pre drug assessments showed that an average of 11.2 level of fatigue showing no significant difference.

In making comparisons of different intrinsic β-blockers influence on cardiovascular patients, has shown that the different antagonists portray similar effect on cardiovascular activity. [ix] When used with exercise therapy, these results showed that it lowered significantly the heart beat rates. Exercise has been predominalty been used in testing the effect of treatment on cardiovascular patients. [x]

Thus this experiment signifies a significant effect of e-adrenoceptor antagonists on exercise induced cardiovascular changes. Beta adrenoceptor has significant effects on the cardiovascular health status, through lowering blood pressure, reducing the levels of heart beat and improved levels of lung function. The different state of physical activity has no significant difference on the effect of beta blockers in binding the receptors of nor epinephrine and epinephrine

References

[i] Audigane, L., Kerfant, B. G., El Harchi, A., Lorenzen?Schmidt, I., Toumaniantz, G., Cantereau, A., ... & Gauthier, C. (2009). Rabbit, a relevant model for the study of cardiac β3?adrenoceptors. Experimental physiology, 94(4), 400-411.

[ii] Bozkurt, B., Bolos, M., Deswal, A., Ather, S., Chan, W., Mann, D. L., & Carabello, B. (2012). New insights into mechanisms of action of carvedilol treatment in chronic heart failure patients—a matter of time for contractility. Journal of cardiac failure, 18(3), 183-193.

[iii] Ferrari, R., Anand, I. S., Ceconi, C., De Giuli, F., Poole-Wilson, P. A., & Harris, P. (1996). Neuroendocrine response to standing and mild exercise in patients with untreated severe congestive heart failure and chronic constrictive pericarditis. Heart, 76(1), 50-55.

[iv] Peller, M., Oziera?ski, K., Balsam, P., Grabowski, M., Filipiak, K. J., & Opolski, G. (2015). Influence of beta-blockers on endothelial function: a meta-analysis of randomized controlled trials. Cardiology journal, 22(6), 708-716.

[v] Billeh, R., Hirsh, D., Barker, C., Jorgensen, B., Jeger, R., Ramanathan, K., ... & Jorde, U. P. (2006). Randomized, Double?Blind Comparison of Acute β1?Blockade With 50 mg Metoprolol Tartrate vs 25 mg Carvedilol in Normal Subjects. Congestive Heart Failure, 12(5), 254-257

[vi] Ladage, D., Schwinger, R. H., & Brixius, K. (2013). Cardio?Selective Beta?Blocker: Pharmacological Evidence and Their Influence on Exercise Capacity. Cardiovascular therapeutics, 31(2), 76-83.

[vii] Marazzi, G., Volterrani, M., Caminiti, G., Iaia, L., Massaro, R., Vitale, C., ... & Rosano, G. (2011). Comparative long term effects of nebivolol and carvedilol in hypertensive heart failure patients. Journal of cardiac failure, 17(9), 703-709.

[viii] Moniotte, S., & Balligand, J. L. (2002). Potential Use of β3?Adrenoceptor Antagonists in Heart Failure Therapy. Cardiovascular Therapeutics, 20(1), 19-26.

[ix] Larochelle, P., Tobe, S. W., & Lacourcière, Y. (2014). β-Blockers in hypertension: studies and meta-analyses over the years. Canadian Journal of Cardiology, 30(5), S16-S2

[x] Yun, S., Vincelette, N. D., & Abraham, I. (2015). Cardioprotective role of β-blockers and angiotensin antagonists in early-onset anthracyclines-induced cardiotoxicity in adult patients: a systematic review and meta-analysis. Postgraduate medical journal, 91(1081), 627-633.

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