Atenolol

Atenolol belongs to the beta-blocker family, more precisely to the second-generation beta-1 adrenergic receptor antagonists described as cardioselective. It binds selectively to the beta-1 receptors of the heart and prevents catecholamines, adrenaline and noradrenaline, from exerting their stimulating effect there. As a result, the heart rate slows, the contractile force of the myocardium decreases and blood pressure falls. Atenolol acts without membrane-stabilizing activity and without intrinsic sympathomimetic activity: it is not a partial agonist, it simply blocks the receptor.

This selectivity for the beta-1 receptors is not absolute: at high doses, a blockade of the beta-2 receptors may appear. Beta-1 blockade does not, moreover, concern only the heart, it also acts on the kidney, where it reduces the secretion of renin, an enzyme that triggers a hormonal cascade increasing blood pressure. This drop in renin contributes to the drug’s antihypertensive effect. Atenolol thus combines two levers, cardiac and renal, to lower pressure.

Atenolol is approved by the health authorities in three main situations: arterial hypertension, angina pectoris (angina) and the acute phase of myocardial infarction. In hypertension, it lowers pressure by slowing the heart and reducing renin. In angina, it decreases the heart’s workload and therefore its oxygen consumption, which spaces out the episodes of chest pain. After an infarction, it protects the weakened myocardium by reducing the adrenergic demand that weighs on it.

Beyond these indications, atenolol is used in situations where its cardiac braking action is sought. Doctors sometimes prescribe it for certain rhythm disorders, for a supraventricular tachycardia, for the prevention of migraine or to control the manifestations of a thyrotoxicosis. These uses fall outside the strict framework of the initial authorization, but they rest on the same pharmacological logic. The choice belongs to the doctor, according to each person’s profile.

Atenolol is taken by mouth, once or twice a day, at a fixed time. Regularity matters: taking the tablet at the same moment each day maintains a stable concentration in the blood. Its elimination half-life, of roughly six to seven hours, explains this rhythm of one to two daily intakes. The treatment is not judged by an immediate sensation, because blood pressure and heart rate are controlled over time, without a signal felt from day to day.

One point is decisive: atenolol must never be stopped abruptly, because a sudden halt can cause a rebound, with an acceleration of the heart and a rise in pressure. Any change goes through the doctor, who reduces the dose gradually if needed. As for its fate in the body, atenolol undergoes little or no transformation by the liver and is eliminated almost entirely by the kidney, through filtration and active secretion, which requires adjusting the dose in case of renal insufficiency. A hydrophilic molecule, it crosses little the barrier that protects the brain, which limits its penetration into the central nervous system.

Fatigue is the most frequent effect: in placebo-controlled studies, it affects 26% of people on atenolol versus 13% on placebo. Then come dizziness or lightheadedness (13% versus 6%), the sensation of cold extremities (12% versus 5%) and depressed mood (12% versus 9%). Shortness of breath concerns 6% of people versus 4% on placebo, and bradycardia, this marked slowing of the heart, 3% versus 0%. Digestive disorders remain rarer: diarrhea 3%, nausea 3%, versus respectively 2% and 1% on placebo.

One effect deserves particular attention in the person with diabetes: atenolol can mask the signs of a hypoglycemia, notably the palpitations and the tremors, those that usually give the alert. It can in the same way mask the signs of a hyperthyroidism. These are not complications in the strict sense, they are warning signals that the drug attenuates and that one must then know how to monitor otherwise. This is one of the reasons why follow-up accompanies the treatment.

The blockade of the beta-1 receptors does not stop at the heart. The pineal gland, in the brain, uses these same receptors to command the manufacture of melatonin, the hormone that opens the night and sets sleep. By blocking them, atenolol reduces the nocturnal secretion of melatonin, an established pharmacological effect. In hypertensive people treated with a beta-blocker, a randomized controlled trial showed that an intake of melatonin improves sleep quality, which is consistent with this decline.

On the plate, melatonin is found only in very small quantities, too low to compensate for the decline the treatment causes. Two other nutrients accompany melatonin in our formula and are found in many foods: magnesium, present in spinach, walnuts, legumes and the banana, and vitamin B6, supplied by salmon, the banana and chickpeas. A link between beta-blockers and coenzyme Q10 is sometimes mentioned, but it remains debated: the older data concern above all lipophilic molecules such as propranolol, and for atenolol, a hydrophilic molecule, they do not allow a depletion to be affirmed. When melatonin production slows under the effect of the drug, food alone does not fill this gap, and this is where a targeted intake takes its meaning, in addition to your treatment, never in its place.

Certain combinations call for caution. With calcium channel blockers, the slowing of the heart can add up and cause a bradycardia or a heart block. On stopping clonidine, atenolol can worsen the rise in pressure, this hypertensive rebound that must be anticipated. Agents that empty the reserves of catecholamines add their hypotensive effect to its own, while non-steroidal anti-inflammatory drugs (NSAIDs) can on the contrary reduce its effect on pressure. Atenolol is moreover contraindicated in case of sinus bradycardia, second- or third-degree atrioventricular block, cardiogenic shock or decompensated heart failure, and it calls for caution in case of asthma or bronchospasm.

Follow-up accompanies the treatment closely. The doctor regularly measures the heart rate and blood pressure, to check that the braking stays in the right range. The doctor evaluates renal function, since it is the kidney that eliminates the molecule and the dose depends directly on it. In the person with diabetes, blood sugar is monitored, all the more since atenolol can blur the signs of a hypoglycemia. This monitoring framework allows the dose to be adjusted and to spot early what needs to be.